Microplastics and nanoplastics are small plastic particles that have significant environmental and health impacts, but they differ in size and behavior.

• Microplastics: There is no officially published definition of microplastics, but in general they are plastic particles that range in size from 1 micrometer (µm) to 5 millimeters (mm). They can be primary microplastics, like microbeads used in cosmetics, or secondary microplastics, which result from the breakdown of larger plastic items. Microplastics are large enough to be seen with the naked eye and can accumulate in various ecosystems, leading to potential ingestion by marine life and humans.
• Nanoplastics: Nanoplastics are much smaller, typically less than 1 µm in size, often in the nanometer scale (1 nm = 0.001 µm). Due to their tiny size, they can penetrate biological membranes more easily, potentially causing more significant health effects. Nanoplastics are challenging to detect and study, making their impact less understood but potentially more hazardous than microplastics.

Microplastics and nanoplastics are pervasive in the environment, originating from a variety of sources that are broadly categorized as primary or secondary.

• Primary Sources: These are plastics intentionally manufactured at a small size. Common examples include microbeads used in cosmetics and personal care products, microfibers from synthetic clothing, and plastic pellets or "nurdles" used in industrial manufacturing. These particles are released directly into the environment through product use or industrial processes.
• Secondary Sources: These originate from the breakdown of larger plastic items such as bottles, bags, and fishing nets. Over time, exposure to sunlight, wind, and water causes these larger plastics to fragment into smaller particles. Secondary microplastics are not intentionally manufactured at their small size but result from the degradation of larger plastic debris.

Mechanisms of Harm to Aquatic Wildlife

1. Physical Impacts:
   • Ingestion and Blockage: Marine animals often mistake microplastics for food, leading to ingestion. Once ingested, these plastics can cause physical blockages in the digestive systems of animals, reducing their ability to absorb nutrients and leading to starvation or malnutrition. For example, sea turtles, fish, and seabirds have been found with stomachs full of plastic, unable to process actual food.
   • Bioaccumulation: Microplastics can accumulate within the bodies of aquatic organisms over time. As these plastics move up the food chain, from prey to predator, they can reach concentrations that are harmful to larger species, including humans who consume seafood.
2. Biological Impacts:
   • Genotoxicity and Cytotoxicity: Microplastics have been shown to cause genetic damage (genotoxicity) and cellular toxicity (cytotoxicity) in aquatic organisms. The physical presence of these particles can disrupt normal cell functions, leading to mutations, cancer, or cell death. Studies have documented DNA damage in fish and invertebrates exposed to microplastics.
   • Oxidative Damage: Microplastics can induce oxidative stress by generating reactive oxygen species (ROS) within cells. This oxidative damage can lead to inflammation, impaired cellular functions, and even apoptosis (programmed cell death). Oxidative stress is a common pathway for toxicity in aquatic organisms exposed to environmental pollutants, including microplastics.
3. Chemical Impacts:
   • Toxicity Pathways: Microplastics often carry harmful chemical additives, such as plasticizers, flame retardants, and heavy metals, which can leach out and enter the tissues of marine animals. These chemicals can disrupt lipid metabolism, leading to energy imbalances and affecting growth and reproduction.
   • Neurotoxicity: The chemicals associated with microplastics can have neurotoxic effects, impairing the nervous system functions of marine animals. This can lead to behavioral changes, such as altered feeding habits, impaired predator-prey responses, and disorientation.

Specific Effects on Aquatic Wildlife

• Reduction of Feeding Activity: Ingestion of microplastics can reduce the feeding activity of marine animals, as their digestive systems become clogged with indigestible particles. This can lead to a decline in energy levels, growth rates, and reproductive success.
• Intestinal Damage: The sharp edges of microplastics can cause physical damage to the intestinal linings of marine organisms, leading to internal injuries, infections, and impaired nutrient absorption.
• Growth Delay: The energy required to process and expel ingested microplastics can detract from the energy available for growth. This results in stunted growth and developmental delays in juvenile marine species.
• Embryotoxicity: Microplastics have been found to impact the development of embryos in marine animals, leading to deformities, reduced hatching success, and impaired survival rates. Embryotoxicity is a critical concern for species with vulnerable early life stages.
• Behavioral Changes: Exposure to microplastics can lead to behavioral changes in marine animals, such as reduced feeding efficiency, altered swimming behavior, and impaired predator avoidance. These changes can have cascading effects on survival and reproductive success.
• Diseases in Marine Animals: Microplastics can serve as vectors for pathogens, carrying harmful bacteria, viruses, and parasites into marine organisms. This can lead to increased incidences of disease, further compromising the health of affected species.

The ecotoxicological effects of microplastics and nanoplastics on aquatic wildlife are not limited to individual organisms. The accumulation of these particles in marine environments can lead to broader ecological disruptions. For example, reduced feeding activity and growth delays in key species can affect the entire food web, leading to declines in predator populations and altering ecosystem dynamics.

Moreover, the persistence of microplastics in the environment means that these impacts can accumulate and intensify over time, potentially leading to long-term declines in biodiversity and the health of marine ecosystems.

The Great Pacific Garbage Patch is a glaring example of how our discarded plastic waste has come to dominate the world's oceans, creating a cycle of pollution that impacts both the environment and human health. As this floating mass of debris continues to grow, so does the urgency to find solutions to the plastic pollution crisis.
​
Microplastics and nanoplastics are not just passive pollutants; they actively harm aquatic wildlife through a variety of mechanisms, including genotoxicity, cytotoxicity, oxidative damage, and neurotoxicity. These impacts, coupled with the physical presence of microplastics in the digestive systems of marine animals, can lead to significant ecological and biological disruptions, underscoring the urgent need for action to reduce plastic pollution in our oceans.

Mason's research, conducted in collaboration with the University of Minnesota, analyzed plastics found in various consumer products including beer, tap water, and salt. They discovered that sea salt is particularly susceptible to plastic contamination due to its production process, which involves evaporating saltwater and leaving behind the solid salt—along with any microplastics present in the water.

Mason emphasized that this contamination is not unique to any one region, stating, "It's not that sea salt in China is worse than sea salt in America, it's that all sea salt—because it's coming from the same origins—is going to have a consistent problem." She urged consumers to reconsider their plastic usage and its pervasive role in our society, suggesting that addressing the flow of plastic into the environment is essential to curbing this widespread contamination.
​
As consumers become more aware of the hidden dangers in everyday products, the need for alternative materials and reduced plastic consumption becomes increasingly critical for both environmental and public health.

A Word on the Benefits of Consuming Salt
Contrary to popular belief, consuming high amounts of salt does not necessarily lead to increased thirst or elevated blood pressure. In fact, studies have consistently failed to support these common assumptions. Instead, elevated insulin levels are the real culprit behind salt retention, which can lead to increased blood pressure. What drives up insulin? Refined sugars and carbohydrates. So, rather than blaming salt, it's more accurate to point the finger at sugar for these issues. Your body requires both sodium and chloride ions, the main components of salt, and it cannot produce them on its own. Therefore, it's essential to obtain these ions through your diet.

If you decide to follow a low-carb diet or engage in fasting, your insulin levels will naturally drop, leading to increased salt excretion through urine. This can cause dizziness, a common symptom when your body lacks adequate salt. The solution? Increase your salt intake. Feeling low on energy? Take salt. Experiencing headaches, brain fog, or difficulty focusing? Salt could be the answer.

Salt is an essential hydration mineral, and not getting enough can negatively impact your quality of life. Unlike some other nutrients, if you consume too much salt, your body simply excretes it through urine. In fact, drinking salt water has been associated with anti-aging properties. Maintaining healthy salt levels can boost your energy, improve sleep quality, reduce muscle cramps, and enhance exercise performance.
​
Starting your day with 16 ounces of water mixed with salt can set you on the right path for maintaining optimal hydration and overall well-being. So, rather than avoiding salt, recognize its vital role in your health and use it wisely to improve your quality of life.

​However, it's important to note that not all salt is created equal. Refined table salt is almost entirely sodium chloride, often with added man-made chemicals. In contrast, unprocessed salts, like pink Himalayan salt, offer a more balanced mix of sodium and chloride, along with other essential minerals such as calcium, potassium, and magnesium. These minerals not only contribute to the pink hue of Himalayan salt but also provide additional health benefits.

Oral Ingestion: Microplastics and nanoplastics enter our bodies predominantly through the food and water we consume. Experimental sampling, such as Fourier-transform infrared spectroscopy (FTIR) on tap, bottled, and spring waters, has confirmed the presence of microplastics in all these sources, highlighting the pervasive nature of this pollution. Studies have detected these particles in everyday items like honey, beer, salt, seafood, and even mineral water. Recent research has shown that a single bottle of water (1L) can contain as many as 240,000 nanoplastic particles. These particles are introduced into the food chain as animals ingest them in their natural environments or as food is contaminated during production processes. Alarmingly, microplastics have also been found in human feces, underscoring their presence in our diet. While the evidence of their presence in food is growing, comprehensive quantitative data on human exposure through diet remains scarce, and no specific legislation currently exists to regulate micro- and nanoscale plastics in foodstuffs.

Inhalation: Airborne microplastics are another significant source of exposure. These particles originate from urban dust, synthetic textiles, rubber tires, and other sources. Due to their small size and lightweight nature, microplastics can remain suspended in the air and be easily inhaled, leading to their deposition in the respiratory system. Research has shown that microplastics can accumulate in the lungs, potentially leading to respiratory issues. More of this down below...

Skin Contact: Although less studied, skin contact represents another potential route of microplastic entry into the body. Microplastics are found in various personal care products, such as exfoliants and cleansers, which can penetrate the skin or be absorbed through wounds. The potential for microplastics to penetrate the skin barrier is an area of active research, with implications for chronic exposure and cumulative health effects.

Recent research has revealed the alarming extent to which humans are exposed to microplastics, with estimates suggesting that we might inhale around 16.2 bits of plastic every hour—equivalent to 5 grams of plastic every week, which is about the weight of a credit card's worth of plastic in just one week. For the first time in history, microplastic particles have been tracked in the lower airways, raising serious concerns about the potential health impacts.
​
Microplastics have been detected in various environments, including the air, water, oceans, lakes, snowfall, and rainfall, according to NOAA researchers. These tiny particles are produced from a wide range of sources, including:

• synthetic materials washed off clothes during laundry cycles, such as polyester and polypropylene
  
• abrasions to vehicle tires or brake components during transportation on the road that cause tiny tire shreds or brake wear particles to fly off
  
• abrasions to everyday plastic or synthetic objects, like the soles of shoes and cooking utensils
  
• runoff from plastic components used to develop and mark roads
  
• coatings used on marine equipment and infrastructure, such as container ships
  
• plastic components used in personal care products, such as plastic microdermabrasion beads in face wash
  
• plastic pellets used in manufacturing

Additionally, microplastics are a byproduct of sewage treatment, where wastewater containing these particles is released into the ocean and then evaporates into the atmosphere in large volumes.

The presence of microplastics in the air is particularly concerning. Microplastics may be present in 4-77% of the air you breathe on a regular basis. Studies have found that microplastics, especially synthetic fibers from textiles, can range in size from 1 to 5 microns—small enough to enter the respiratory system, pass through the lungs, and potentially enter the bloodstream. These particles can damage the air sacs in the lungs, increasing the risk of conditions like emphysema and lung cancer.

A 2020 study in Environment International conducted in London found that the air samples collected from the top of a 9-story building contained between 575 to 1008 microplastics per square meter. The study also suggested that microplastics could travel great distances through wind and weather patterns, potentially reaching remote areas like the North Atlantic and the Arctic during certain seasonal conditions like the North Atlantic Oscillation (NAO).

This growing body of research underscores the pervasive nature of microplastic pollution and the urgent need for further studies to understand the full extent of their impact on human health and the environment.

Over time, the exposure to plastic really adds up. According to the World Wildlife Federation’s calculations, each month, you consume about 21 grams, or the equivalent of one Lego brick. In a year’s time, you’ve consumed 250 grams, or the size of a full dinner plate’s-worth of plastic.

In 10 years, you’ve ingested some 5.5 pounds, and in the average lifetime, a person will consume about 40 pounds. While much of this will pass through and be eliminated through your stool, some will remain and accumulate in your organs.

Recent research has uncovered alarming insights into the effects of weathered microplastics on human health, particularly concerning brain cells. Unlike newly manufactured plastics, weathered microplastics—those degraded by environmental factors such as heat and light—have been shown to trigger a more severe inflammatory response in human brain cells.

In an experiment led by Hee-Yeon Kim and colleagues at the Daegu Gyeongbuk Institute of Science and Technology (DGIST), researchers exposed microglia, the brain's immune cells, to weathered polystyrene microplastics. These plastics, which had undergone environmental degradation, caused a dramatic increase in inflammatory particles in the blood of mice. Additionally, there was a marked increase in brain cell death compared to those exposed to "virgin" or new microplastics.

The study found that weathered microplastics altered the expression (by a factor of 10-15) of proteins involved in energy metabolism and significantly increased proteins associated with brain cell death by a factor of five. The team suggests that these effects might be due to changes microplastics undergo when exposed to sunlight and UV radiation, such as increased brittleness and fragmentation, leading to a larger surface area and altered chemical bonds that heighten their reactivity.

This all amounts to an increased inflammatory response by brain cells — far more severe than what was produced by unweathered microplastics tested at equivalent doses.

This discovery has significant implications for human health, especially considering that much of the microplastic we consume comes from food sources. As plastic waste in the oceans breaks down into microplastics through exposure to sunlight, these particles are ingested by marine life, which then enters the human food chain. The increased neurotoxic potential of weathered microplastics emphasizes the urgent need for further research and potential policy interventions to mitigate the impact of microplastics on human health.

Recent research has highlighted the alarming effects of polystyrene nanoplastics (PS NPs) on cardiovascular health, specifically in the context of lipid accumulation and atherosclerosis. The study demonstrated that exposure to PS NPs, especially when combined with oxidized low-density lipoprotein (ox-LDL), led to significant lipid buildup in RAW264.7 macrophages. This lipid accumulation is a key marker in the development of atherosclerosis, a condition characterized by the hardening and narrowing of arteries due to plaque formation.

Using ultrasound biomicroscopy (UBM), researchers observed the development of atherosclerotic plaques in the aortic arch of ApoE-/- mice after three months of PS NPs exposure. This was further confirmed by Oil-red O and hematoxylin-eosin (H&E) staining, which revealed lipid deposition and plaque formation in the aortic root of these mice.

The study also linked the development of atherosclerosis in these mice to disturbances in lipid metabolism and oxidative stress damage in the liver. This suggests that PS NPs exposure not only affects local cardiovascular structures but also has systemic implications, disrupting lipid regulation and promoting inflammation.
​
These findings underscore the potential cardiovascular risks posed by nanoplastic exposure. Atherosclerosis, closely associated with abnormal lipid metabolism and oxidative stress, is a significant contributor to heart disease. The study indicates that PS NPs might exacerbate these processes, raising concerns about their long-term impact on cardiovascular health.

In a study published in the International Journal of Molecular Sciences, researchers uncovered the cytotoxic effects of microplastics on human cells. The study demonstrated that microplastic particles are capable of entering cells within just 24 hours of exposure, where they predominantly accumulate around the cell nucleus. This rapid infiltration is concerning, as it directly impacts cell health. The study showed that as the concentration of microplastics and the duration of exposure increased, cell viability—meaning the ability of cells to survive—significantly decreased.

Additionally, the study observed alarming changes in immune response markers. Notably, the expression of tumor necrosis factor (TNF-a), a cytokine involved in inflammation, was found to be twice as high in the livers of mice exposed to microplastics compared to those that were not exposed. This suggests that microplastics not only harm individual cells but can also trigger broader immune responses, potentially leading to inflammation and other related health issues.

These findings add to the growing body of evidence that microplastics pose serious health risks, emphasizing the need for further research and public awareness regarding their pervasive presence in our environment and food supply.

Micro- and nanoplastics have been shown to cause liver inflammation, a critical concern as the liver is essential for detoxifying the body. These plastics disrupt mitochondrial membrane potential, which is stronger with 5 μm particles, inhibiting ATP production—a crucial energy source for cells. Additionally, MNPs negatively affect food absorption and digestion, leading to altered hepatic lipid metabolism. This can result in changes in cholesterol and triglyceride (serum and total cholesterol, serum and total triglycerides, HDL and LDL) levels, which are risk factors for cardiovascular diseases.

MNPs can severely affect the gastrointestinal system. They negatively affect food absorption, inhibit food digestion, decrease mucus secretion in the intestine and impair gut microbiota composition, essential for a healthy digestive system. The dysfunction of the intestinal barrier caused by MNPs can lead to gut dysbiosis and impaired bile acid metabolism, further contributing to digestive issues and metabolic disorders.

Nanoplastics, due to their tiny size (the smaller the more harmful), pose a significant threat to the brain. These particles can cross the blood-brain barrier (BBB) within just two hours, a crucial defense that protects the brain from harmful substances. Once they breach the BBB, they can lead to cognitive impairment, neurological disorders, and neurotoxicity. This neurotoxic effect is thought to be due to the inhibition of acetylcholinesterase activity and altered neurotransmitter levels, which can contribute to behavioral changes. The high surface area to volume ratio of these particles makes them particularly reactive and potentially more harmful than larger microplastics.

​Experimental studies have shown that MNPs absorbed into cholesterol molecules on the brain membrane surface can cross the BBB and increase the risk of inflammation and neurological disorders. This could potentially contribute to neurodegenerative diseases such as Alzheimer’s and Parkinson’s. The plastic microparticles in the brain could induce neuroinflammation, leading to long-term damage and chronic neurological conditions.

​In a study published in the August 2023 issue of the International Journal of Molecular Sciences, researchers uncovered alarming evidence that microplastics extensively infiltrate the body, including the brain, and can induce behavioral changes reminiscent of dementia in as little as three weeks. This research involved exposing both young (4-month-old) and old (21-month-old) mice to varying levels of microplastics in their drinking water over a three-week period.

Behavioral testing at the conclusion of the study revealed that many of the mice exhibited dementia-like symptoms, with older animals showing more pronounced changes. The researchers theorized that age-related dysfunction might exacerbate the effects of polystyrene microplastics (PS-MPs) on behavioral performance. Lead researcher Jaime Ross described the findings as "striking" because the doses of microplastics administered were relatively low.

Upon dissecting the animals, the researchers discovered that microplastics had accumulated in every organ, including the brain, which was an unexpected and shocking finding. Although the presence of microplastics in the gastrointestinal tract, liver, and kidneys was anticipated, their expansion to other tissues, such as the heart and lungs, suggests that microplastics are capable of undergoing systemic circulation.

Of particular concern was the detection of microplastics in the brain, which should be protected by the blood-brain barrier, a mechanism designed to prevent harmful substances, including bacteria and viruses, from entering the brain. The presence of microplastics in brain tissue raises significant concerns, as it may lead to a decrease in glial fibrillary acidic protein (GFAP), a protein that supports cell processes in the brain. A reduction in GFAP has been associated with the early stages of neurodegenerative diseases, such as Alzheimer's disease, and even depression.

The study further explained that GFAP is commonly used as a marker for neuroinflammation and is typically found in mature astrocytes, which are cells located in the brain and spinal cord, and is involved in cellular processes such as autophagy, neurotransmitter uptake and astrocyte development. Although inflammation is usually linked to increased GFAP levels, the researchers observed a slight decrease in GFAP expression in the microplastic-exposed mice. This finding aligns with previous studies suggesting that early stages of certain diseases might be characterized by astrocyte atrophy, leading to decreased GFAP expression.
​
These findings underscore the potential for microplastics to contribute to neurological damage and cognitive decline, emphasizing the need for further research to fully understand the implications for human health.

Microplastics, increasingly recognized as endocrine disruptors, are now believed to be present in the majority of people. These tiny particles can cause structural changes and physical damage in the body, potentially long before their long-term endocrine effects have a chance to accumulate and cause harm on their own. One of the most concerning impacts of microplastics is their potential role in male infertility.
​
Many products, particularly canned and plastic goods, are high in synthetic forms of estrogen, such as bisphenol A (BPA). BPA, a well-known xenoestrogen, is notorious for leaching from polycarbonate plastics into food and drinks, especially when exposed to heat. This exposure can lead to various health issues, including alterations in liver function, insulin resistance, damage to developing fetuses, and modifications in reproductive and neurological functions.

Environmental toxins, including microplastics, are capable of penetrating the testicle and semen, potentially leading to deleterious effects on testicular function. This includes impairing testosterone production and sperm production, both of which are critical for male and female fertility. Research indicates that male factor infertility contributes to 50% of all infertility cases and is the sole cause in 20-30% of cases. The presence of microplastics and other endocrine-disrupting chemicals in the environment is increasingly seen as a significant factor in this rising trend.

Moreover, BPA and similar chemicals act as agonists for estrogen receptors, inhibiting thyroid hormone-mediated transcription, altering pancreatic beta cell function, and increasing the likelihood of obesity, cardiovascular diseases, and reproductive issues. The pervasive nature of these toxins in Western civilization underscores the urgent need to address their impact on human health, particularly concerning male fertility and overall endocrine function.
​
This segment highlights the pressing concern that environmental pollutants like microplastics pose to human health, particularly through their role as endocrine disruptors and their potential contribution to the growing issue of male infertility.

Research has increasingly shown that these tiny plastic particles can induce severe biological effects that span multiple generations and trigger various health conditions, including cancer.

In vitro studies have demonstrated that polystyrene nanoparticles (PS NPs) can induce oxidative stress, which leads to cellular damage in a context-dependent manner. This oxidative stress can result in apoptosis (programmed cell death) and autophagic cell death, processes that can significantly impact the health of exposed organisms.

Research using zebrafish models has provided alarming insights into the long-term effects of PS exposure. Zebrafish injected with 20 nm-sized PS particles during their embryonic stage and later grown in a plastic-free environment still passed on significant health issues to their offspring. The affected offspring exhibited malformations, decreased survival rates, increased heart and blood flow rates, and impaired growth, including smaller eye size and reduced locomotor activity. These effects were linked to increased cell death, elevated reactive oxygen species, and decreased lipid accumulation in the larvae. This study highlights the potential for PS exposure to disrupt biological processes across generations and contribute to disease development, including cancer.

BPA, an endocrine-disrupting chemical widely used in plastic manufacturing, has been identified as a possible risk factor for developing breast cancer. BPA has a strong affinity for non-classical membrane estrogen receptors, such as G protein-coupled receptors (GPER), and can alter multiple molecular pathways within cells (estrogen-related receptor gamma (ERRγ) pathway, HOXB9 (homeobox-containing gene) pathway, bone morphogenetic protein 2 (BMP2) and (BMP4), immunoregulatory cytokine disturbance in the mammary gland). These changes include disruptions in the EGFR-STAT3 pathway, FOXA1 in estrogen receptor-negative breast cancer cells, and epigenetic modifications through the enhancer of zeste homolog 2 (EZH2). These molecular alterations can lead to the undesired stimulation or repression of genes, increasing the risk of developing breast cancer.

The evidence linking MNP exposure to significant health risks is growing. From inducing oxidative stress and cell death to potentially triggering transgenerational effects and increasing the risk of breast cancer, the implications of MNP exposure are profound. Limiting exposure to these harmful particles, especially BPA, is crucial in reducing the risk of developing serious health conditions, including cancer.

In a groundbreaking study published in IJIR: Your Sexual Medicine Journal, microplastics have been discovered for the first time in human penile tissue. This discovery raises concerns about a potential link between microplastics and erectile dysfunction (ED), opening up new avenues of research into the impact of environmental pollutants on male sexual health.

The study, highlighted by CNN Health, analyzed tissue samples from five men undergoing penile implant surgery for ED at the University of Miami. Astonishingly, four out of the five samples contained microplastics, with polyethylene terephthalate (PET) and polypropylene (PP) being the most common types found.

Ranjith Ramasamy, the study’s lead author and a reproductive urology expert, explained, "The presence of microplastics in the penis is unsurprising. The penis, like the heart, is a highly vascular organ." This observation underscores the potential risk that microplastics pose to vascular-rich organs, but the connection between these particles and ED remains uncertain.

Male infertility remains a global issue, with its causes often not well understood. Given the growing evidence of microplastics infiltrating various biological systems, such as blood and lungs, researchers are now exploring their potential effects on reproductive systems. Previous research has investigated the presence of microplastics in male reproductive organs. For example, in one study, researchers discovered 12 different types of microplastics in the testicles of dogs and humans. In dogs, they found that higher levels of certain microplastics correlated with lower sperm counts and reduced testis weight.

Further research is essential to determine whether microplastics contribute to ED or other health issues. According to Ramasamy, "We need to identify if microplastics are linked to ED and if there are specific types or quantities that cause harm." The discovery marks the beginning of what could be a critical exploration into how microplastics may affect male sexual function and overall health.
​
As the scientific community continues to investigate, this study highlights the growing concern over the pervasive presence of microplastics in the human body and their potential implications for health, particularly in sensitive and vital tissues such as those involved in sexual function.

The study of microplastics and nanoplastics is fraught with challenges and complexities that make it difficult to fully understand their impact on the environment and human health. One of the main obstacles is the sheer diversity and complexity of these plastic particles. Micro- and nanoplastics are not a single type of material but rather a complex mixture of various polymers, additives, and contaminants. This diversity complicates efforts to develop standardized methods for detecting and analyzing these particles.

To minimize your contribution to global microplastics pollution, it's essential to make conscious decisions about the plastic products you buy and how you dispose of them. The pervasive issue of microplastics begins with the widespread use of cheap, disposable plastic items that are used once and immediately discarded. With nearly 8 billion people on the planet, this behavior results in an immense amount of plastic waste being generated every day. 
​
One of the most effective steps you can take is to choose recyclable plastic goods and recycle them correctly. Look for the universal recycling logo, often marked with a number inside the symbol. With approximately 299 million tons of plastic produced annually, these codes help identify how safe the plastic is, its environmental impact, and its recyclability. This number, known as the resin identification code, identifies the type of plastic and its recyclability. Here's a breakdown of common plastics and how to handle them:

• Polyethylene Terephthalate (PET, Plastic #1): Found in clear beverage bottles, synthetic fibers, and food packaging. PET is recyclable but should not be reused, especially if exposed to heat, as it can leach harmful chemicals, like antimony trioxide and DEHA, to leach into your liquids. Avoid reusing these containers as their porous nature can harbor bacteria.
• High-Density Polyethylene (HDPE, Plastic #2): Used in milk jugs, detergent bottles, and piping. HDPE is opaque, widely recyclable and considered one of the safer plastics. It has a low risk of leaching harmful substances and is widely accepted by recycling programs.
• Polyvinyl Chloride (PVC, Plastic #3): Common in plumbing pipes, cable insulation, medical tubing, and window frames, PVC is not recyclable and should be avoided, particularly for food-related use due to its harmful chemical (phthalates, dioxins, etc.) content which interfere with hormonal development.
• Low-Density Polyethylene (LDPE, Plastic #4): Found in grocery bags, containers, squeezable bottles and some food wraps, LDPE is difficult to recycle. It's better to reuse these items or switch to alternatives like reusable bags. Significant environmental impact.
• Polypropylene (PP, Plastic #5): Used in food containers, automotive parts, textiles, and medical devices, and yogurt cups, PP is generally safe and recyclable in many areas.
• Polystyrene (PS, Plastic #6): Used for disposable cutlery, food containers (foam plates/cups), foam packaging (Styrofoam, packing peanuts), and insulation materials, PS is notoriously difficult to recycle and can leach carcinogenic chemicals (styrene), especially when heated. It's best to avoid using PS altogether. It can take hundreds of years to decompose. 
• Other (Plastic #7): This category includes a variety of plastics (new/mixed plastics, LEXAN, etc.) that are often difficult to recycle and may contain harmful chemicals like BPA. Use products in this category with caution. Some are recyclable and some are not.
  • Polycarbonate (PC): Used in eyewear lenses, DVDs, automotive parts, and reusable water bottles. Should generally be avoided, especially in food and drink containers due to their potential to leach harmful chemicals. 
  • Acrylonitrile Butadiene Styrene (ABS): Found in LEGO bricks, automotive parts, and consumer electronics. It's environmental impact due to poor recyclability is concerning.
  • Polyamide (Nylon): Used in textiles, automotive parts, and industrial components.
  • Polytetrafluoroethylene (PTFE): Known as Teflon, used in non-stick cookware, plumbing tape, and industrial applications.
  • Polylactic Acid (PLA): A biodegradable plastic made from renewable resources like corn starch, used in disposable cups, packaging, and 3D printing. It’s still not perfect for high-temperature environments, as it can deform or release lactic acid under heat.

A 2020 review in Earth-Science Reviews identified microplastics in air pollution as potentially the largest contributor to microplastic contamination worldwide, affecting even remote regions like the Arctic and the vast expanses of our oceans. The pervasive nature of microplastics in the atmosphere is alarming, as these particles are not only inhaled but also deposited on land and water surfaces through precipitation, leading to widespread environmental and health impacts.
​
However, there are steps individuals can take to mitigate their exposure to microplastics and reduce their environmental footprint:

1. Opt for Compostable or Biodegradable Products: Traditional plastics are made from synthetic materials that can take thousands of years to degrade. Products labeled as compostable or biodegradable are designed to break down more quickly, either by decomposing in the soil or being consumed by microorganisms. Examples of rapidly degrading materials include starch-based polymers, plant-based silvergrass, wood fiber, and coconut fiber.
2. Avoid Harmful Plastic Substitutes: While it's beneficial to reduce single-use plastics, not all alternatives are created equal. For instance, "biodegradable" plastic bottles or bags may still take years to break down and could release harmful chemicals during degradation. Similarly, bamboo products (straws and silverware), though sustainable in small quantities, could become problematic if demand leads to over-harvesting of bamboo forests. Re-used plastic (clothes or shoes made of “recovered” plastic) still keeps plastic in the manufacturing and consumption cycle, leading to further environmental pollution by microplastics
3. Consider Durable, Eco-Friendly Alternatives: Many companies now offer long-lasting alternatives to plastic, such as glass or stainless steel products. Though initially more expensive, these materials do not generate microplastics and can endure years of use. For example, using stainless steel or glass containers instead of plastic can significantly reduce microplastic exposure, especially when heating food or beverages.

Reducing plastic consumption and waste generation is an effective strategy. Simple steps like using reusable shopping bags, using your own coffee mug when getting coffee to go, avoiding plastic-wrapped dry cleaning, ​bringing drinking water from home in glass water bottles instead of buying bottled water, and store foods in glassware or mason jars instead of plastic bags. You can also take your own leftover container to restaurants, which can significantly cut down the amount of plastic that ends up in landfills and oceans, thereby decreasing the microplastic contamination in our food and water. 

​Strategies such as these will help to reduce the amount of plastic that can migrate into your food.  Plastic is all around us and can be extremely difficult to avoid. But if you start looking around, you may find many areas of your life where you can eliminate the use of plastic and replace the it with something inert that won’t harm the environment and your health.

Given that adults may ingest thousands of microplastics annually through water consumption alone, it is advisable to minimize the use of plastic water bottles. Opting for a non-plastic water container, like one made from stainless steel or copper, can significantly reduce this exposure. Additionally, experts recommend avoiding microwaving food in plastic containers or placing them in the dishwasher, as heat can cause more plastic to leach into food, and release into the environment.

These changes, while seemingly small, can collectively make a significant difference in reducing microplastic pollution and protecting both human health and the environment.

In the battle against plastic pollution, both businesses and individuals play crucial roles. One initiative that stands out is the B Corporation movement. B Corporations are businesses committed to reducing global waste and promoting fair hiring and manufacturing practices across their supply chains. These companies actively work to minimize the use of materials that generate microplastics, making them leaders in sustainability. When shopping, look for the B Corporation logo—a "B" encircled—to support companies that adhere to these eco-friendly standards.

On an individual level, protecting yourself from airborne microplastics is becoming increasingly important. Microplastic particles in the air, though often larger than typical pollutants like PM10 and PM2.5, still pose significant health risks. Thankfully, these larger particles are easier to capture with a high-performance air purifier.

​While many air purifiers can only trap smaller pollutants, high-performance models with centrifugal fans are specifically designed to capture even large and heavy microplastics. These purifiers filter out particles as small as 0.003 microns, which is far smaller than the tiniest microplastics.

Consider using a personal air purifier in spaces where microplastics are likely to accumulate, such as bedrooms or workspaces, where they can be emitted from clothing, appliances, and containers. Additionally, a car air purifier can help filter out microplastics from tire and brake wear, which can infiltrate your vehicle's interior, especially in high-traffic areas.

​Emerging research suggests that sweating, whether through exercise or sauna use, may play a role in detoxifying the body from accrued microplastics. A 2022 study detected microplastic particles such as polyethylene, PET, and polymers from sportswear in sweat collected after exercise, indicating that perspiration could aid in the elimination of these particles alongside other toxins like pesticides, flame retardants, and bisphenol-A. This adds to a growing body of evidence showing that sweating can facilitate the excretion of heavy metals, petrochemicals, and other pollutants.
​
As with other toxins, microparticle content in sweat could indicate efficacy of interventions promoting clearance. Given the increasing prevalence of microplastics in our environment, inducing sweat through regular sauna use or exercise could offer a simple and accessible detoxification method to help reduce the body's burden of microplastics. However, more research is needed to understand the full impact of repeated sweating on microplastic levels in the body. Additionally, regulatory limits specific to nanoplastics in food and drinks could help safeguard public health given the unprecedented exposure uncovered by advanced microscopy techniques. After all, "seeing" the risk is the first step toward safety.

Obesogens, through their pervasive presence in our environment, exert insidious effects on metabolic function, including the intricate workings of mitochondria – the cellular powerhouses responsible for energy production. By disrupting mitochondrial function, obesogens can contribute to metabolic dysregulation and, ultimately, weight gain.

Mitochondria play a central role in energy metabolism, converting nutrients into adenosine triphosphate (ATP), the primary source of cellular energy. However, exposure to obesogens can impair mitochondrial function through various mechanisms, including:

• Oxidative Stress: Obesogens can promote the generation of reactive oxygen species (ROS) within mitochondria, leading to oxidative damage and dysfunction.
• Mitochondrial Biogenesis: Some obesogens interfere with the process of mitochondrial biogenesis, the creation of new mitochondria, which is essential for maintaining optimal energy metabolism.
• Respiratory Chain Dysfunction: Obesogens may disrupt the electron transport chain, a series of protein complexes within mitochondria that generate ATP, impairing energy production.
• Mitochondrial Membrane Integrity: Obesogens can compromise the integrity of mitochondrial membranes, affecting the transport of ions and molecules critical for energy production.

​The disruption of mitochondrial function by obesogens can have profound implications for metabolic health and contribute to obesity through several pathways:

1. Impaired Energy Expenditure: Dysfunctional mitochondria are less efficient at generating ATP, leading to reduced energy expenditure and a propensity for weight gain.
2. Insulin Resistance: Mitochondrial dysfunction can impair insulin signaling pathways, contributing to insulin resistance, a hallmark of obesity and metabolic syndrome.
3. Altered Lipid Metabolism: Mitochondria play a crucial role in lipid metabolism, including the breakdown of fatty acids for energy. Disrupted mitochondrial function can lead to aberrant lipid accumulation and adipogenesis, contributing to obesity.

The impact of obesogens on human health extends beyond weight gain, with associations documented with various health conditions, including:

• Obesity: Obesogens have been implicated in the global obesity epidemic, contributing to excess weight gain and adiposity. This includes being overweight, abdominal obesity (midsection fat), childhood and adult obesity.
• Insulin Resistance and Diabetes: Disruption of metabolic pathways by obesogens can lead to insulin resistance, a precursor to type 2 diabetes.
• Fatty Liver Disease: Chemical exposures, including those to bisphenols and phthalates, have been linked to the development of non-alcoholic fatty liver disease (NAFLD).

Additionally, obesogens are highly related to the following health conditions and physiologic imbalances:

Relatively little is known about the extent to which obesogen exposure programs dysfunctional adipose tissue that may store but not mobilize fat. However, emerging evidence suggests that obesogens may contribute to adipocyte dysfunction, leading to altered fat storage and metabolism. One potential underlying factor is suboptimal liver detoxification pathways due to inadequate micronutrient cofactors.
​
Inadequate levels of essential micronutrients, such as vitamins and minerals, can impair liver detoxification pathways responsible for metabolizing and eliminating obesogens from the body. As a result, obesogens may accumulate in adipose tissue, disrupting metabolic function and contributing to weight gain. Additionally, micronutrient deficiencies can compromise mitochondrial function, further exacerbating metabolic dysfunction and obesity risk.​

In the quest for weight loss, many of us often find ourselves fixating on calorie counting, fad diets, or intense workout regimens. However, what if I told you that the key to achieving a healthy weight isn't solely about shedding pounds but rather fixing your metabolism? Enter obesogens – a lesser-known yet influential factor in the obesity epidemic.

As mentioned, obesogens are chemicals found in our environment, ranging from pesticides and plastics to food additives and personal care products. These substances have the uncanny ability to disrupt our body's natural weight-regulating mechanisms, leading to weight gain and metabolic dysfunction. Instead of solely blaming calories in versus calories out, it's essential to recognize the role obesogens play in shaping our metabolism.

2. Consume Micronutrients: Vital micronutrients, such as vitamins and minerals, serve as essential cofactors in metabolic pathways. Ensuring adequate intake of these micronutrients through a balanced diet rich in fruits, vegetables, whole grains, and lean proteins can support optimal metabolic function. Additionally, supplementation may be necessary to address any deficiencies and promote metabolic health.
​
The conventional approach to weight loss often overlooks the critical role obesogens play in metabolic dysfunction. Instead of solely focusing on calorie restriction or intense exercise, shifting our focus to fixing metabolism through toxin reduction and micronutrient consumption offers a more holistic and sustainable solution to achieving optimal health. By addressing the underlying factors contributing to metabolic disruption, we can pave the way for lasting weight management and overall well-being.

Online/In-Person Guidance
One of the standout features of the Integral Wellness Program is its flexibility, offering both online and in-person consultations tailored to individual preferences and needs. Whether you prefer the convenience of virtual sessions or the hands-on approach of in-person coaching, our team of experienced wellness professionals is dedicated to supporting you every step of the way.

The environment that we live in is toxic. It is worrisome to think that the status quo has occurred with the help of corporations knowingly dumping harmful chemicals into the environment.

The Environmental Working Group (EWG) has studied the current state of our world in great detail and has discovered that before a child is even born they already have approximately 287 toxins in their blood and tissues. These results came from 10 newborns whose parents gave permission to have their toxins measured at birth.

The results of this study indicate that an average of 200 chemicals was found in each newborn. Of the toxins tested, 47 were consumer ingredients such as cosmetics, 212 were industrial and pesticide byproducts. In this study, only around 400 total chemicals were actually tested for - thousands of others may have been found if larger parameters were used.

Many of the toxins measured in the newborns included plastics, flame retardants, and other chemicals that disrupt brain function, IQ, hormones, and the nervous system of the child. Some of the toxins observed like DDT, have actually been banned since 1972 (over 3 decades ago), but are still being measured in laboratory samples. Certain chemicals never fully degrade in the environment.

So, there is not question about it, the environment we live in is toxic. All of us have disease-creating toxins inside of our bodies, the question boils down to which ones and how much.

But there are some solutions: lab tests and detoxification.

More than 2000 references on the biological responses to radio frequency (RF) and microwave radiation, published up to June 1971, have been well-documented by the U.S. Naval Medical Research Institute. Devices that emit RF and microwave radiation include, but is not limited to, cellphones, two-way radios, Wi-Fi routers, cellphone towers, smart watches, bluetooth devices, Smart meters, cordless cell phone base stations, wireless baby monitors, microwave ovens, and any WiFi-connected smart devices that receives and transmits data. Particular attention has been paid to the effects on man of non-ionizing radiation at these frequencies.

Reported Biological Phenomena (*Effects') and Some Clinical Manifestations Attributed to Microwave and Radio-Frequency Radiation

A. Heating of Organs*
(Applications: Diathermy, Electrosurgery, Electro-coagulation, Electrodesiccation, Electrotomy)

1. Whole Body (temperature regulation defects), Hyperpyrexia
2. Skin
3. Bone and Bone marrow
4. (a) Lens of Lye (cataractous lesions - due to the avascular nature of the lens which prevents adequate heat dissipation (b) Corneal damage also possible at extremely high frequencies
5. Cenitalia (tubular degeneration of testicles)
6. Brain
7. Sinuses
8. Metal Implants (burns near hip pins, etc.)

The effects are generally reversible except for 4a.

B.  Changes in physiologic function

1. Striated Muscle Contraction
2. Alteration of Diameter of Blood Vessels (increased Vascular elasticity, Dilation
3. Changes in Oxidative Processes in Tissues and Organs
4. Liver Enlargement
5. Altered Sensitivity to Drug Stimuli
6. Decreased Spermatogenesis (decreased fertility, to sterility)
7. Altered Sex Ratio of Births (more girls!)
8. Altered Menstrual Activity
9. Altered Fetal Development
10. Increased Lactation in Nursing Mothers
11. Reduction in Piuresis (Na+ excretion, via urine output)
12. Altered Renal function (decreased filtration in tubules)
13. Changes in Conditioned Reflexes
14. Increased Electrical Resistance of Skin
15. Changes in the Structure of Skin receptors of the (a) Digestive, and  (b) Blood Carrying Systems
16. Altered BIood Flow Rate
17. Alterations In the Biocurrents (EEG?) of the Cerebral Cortex (in animals)
18. Changes In the Rate of Clearance of Tagged Ions from Tissue
19. Reversible Structural Changes In the Cerebral Cortex and the Diencephalon
20. Electrocardiographic (EKG) Changes
21. Alterations In Sensitivity to Light, Sound, and Olfactory Stimuli
22. Functional (a) and Pathological (b) Changes in the Eyes: (a) decrease in size of blind spot, altered color recognition, changes in intraocular pressure, lacrimation, trembling of eye-lids; (b) less opacity and coagulation, altered tissue respiration, and altered reduction-oxidation processes
23. Myocardial Necrosis
24. Hemorrhage in Lungs, Liver, Gut, and Brain (At Fatal Levels of Radiation)
25. Generalized Degeneration of all Body Tissue of Radiation (At Fatal Levels of Radiation)
26. Loss of Anatomical Parts
27. Death
28. Dehydration
29. Altered Rate of Calcification of Certain Tissue

C.  Central Nervous System Effects

1. Headaches
2. Insomnia
3. Restlessness (Awake and During Sleep)
4. Electroencephalographic (EEG) Changes
5. Cranial Nerve Disorders
6. Pyramidal Tract Lesions
7. Conditioned Reflex Disorders
8. Vagomimetic Action of the Heart; Sympaticomimetic Action
9. Seizures, Convulsions

D.  Autonomic Nervous System Effects

1. Degenerative Disorders (e.g., alteration of heart rhythm)
2. Fatigue
3. Structural Alterations in the Synapses of the Vagus Nerve
4. Stimulation of Parasympathetic Nervous System (Bradycardia), and Inhibition of  the Sympathetic Nervous System

E.  Peripheral Nervous System Effects

1. Effects on Locomotor Nerves

F. Psychological Disorders ("Human Behavioral Studies") - the so-called "Psychophysiologic (and Psychosomatic) Responses"

1. Neurasthenia - (general "bad" feeling)
2. Depression
3. Impotence
4. Anxiety
5. Lack of Concentration
6. Hypochondria
7. Dizziness
8. Hallucinations
9. Sleepiness
10. Insomnia
11. Increased Irritability
12. Decreased Appetite
13. Loss of Memory
14. Scalp Sensations
15. Increased Fatigability
16. Chest pain
17. Tremor of the hand

G. Behavioral Changes (Animal)

1. Reflexive, Operant, Avoidance, and Discrimination Behaviors

H. Blood Disorders
changes in:

1. Blood and Bone Marrow
2. Phagocytic (polymorphs) and Bactericidal Functions
3. Hemolysis Rate (increase), (a shortened lifespan of cells)
4. Sedimentation Rate (increase), due to changes in serum concentration levels or amount of fibrinogen. (?))
5. Number of Erythrocytes (decrease), also number of lymphocytes
6. Blood Glucose Concentration (increase)
7. Blood Histamine Content
8. Cholesterol and Lipids
9. Gamma (also alpha and beta) Globulin, and Total Protein Concetration
10. Number of Eosinophils
11. Albumin/Globulin Ratio (decrease)
12. Hemopoiesis (rate of formation of blood corpuscles)
13. Leukopenia (increase in number of white cells), and Leukocytosis
14. Reticulocytosis

I. Vascular Disorders

1. Thrombosis
2. Hypertension

J. Enzyme and Other Biochemical Changes
Changes in activity of:

1. Cholinesterase
2. Phosphatase
3. Transaminase
4. Amylase
5. Carboxydismutase
6. Protein Denaturation
7. Toxin, Fungus, and Virus Inactivation (at high radiation dose levels), Bacteriostatic  Effect
8. Tissue Cultures Killed
9. Alteration In Rate of Cell Division
10. Increased Concentration of RNA in Lymphocytes, and Decreased Concentration in  Brain.  Liver,  and  Spleen
11. Changes in Pyruvic Acid, Lactic Acid, and Creatinine Excretions
12. Change in Concentration of Glycogen in Liver (Hlyperglycemia)
13. Alteration in Concentration of 17- Ketosteroids in Urine

K. Metabolic Disorders

1. Glycosuria (sugar in urine; related with blood sugar?)
2. Increase in Urinary Phenol (derivatives? DOPA?)
3. Alteration of rate of metabolic Enzymatic Processes
4. Altered Carbohydrate Metabolism

L. Gastro-Intestinal Disorders

1. Anorexia (loss of appetite)
2. Epigastric Pain
3. Constipation
4. Altered Secretion of Stomach "Digestive Juices"

M. Endocrine  Gland  Changes

1. Altered Pituitary Function
2. Hyperthyroidism
3. Thyroid Enlargement
4. Increased Uptake of Radioactive Iodine by Thyroid Gland
5. Altered Adrenal Cortex Activity
6. Decreased Corticosteroids in Blood
7. Decreased Glucocorticoidal Activity
8. Hypogonadism (usually decreased testosterone production)

N. Histological Changes

1. Changes in Tubular Epithelium of Testicles
2. Gross Changes

O. Genetic and Chromosomal Changes

1. Chromosome Aberrations (e.g., linear shortening, pseudochiasm, diploid structures, amitotic division, bridging, "sticky" chromosomes, irregularities in chromosomal envelope)
2. Mutations
3. Mongolism
4. Somatic Alterations (changes in cell not involving nucleus or chromosomes, cellular transformation)
5. Neoplastic Diseases (e.g*, tumors)

P. Pearl Chain Effect (Intracellular orientation of subcellular particles, and orientation of cellular and other (non-biologic) particles) Also, orientation of animals, birds, and fish in electromagnetic fields

Q. Miscellaneous Effects

1. Sparking between dental fillings
2. Peculiar metallic taste in mouth
3. Changes in Optical Activity of Colloidal Solutions
4. Treatment for Syphilis, Poliomyelitis, Skin Diseases
5. Loss of Hair
6. Brittleness of Hair
7. Sensations of Buzzing Vibrations, Pulsations, and Tickling About the Head and Ears
8. Copious Perspiration, Salivation, and Protrusion of Tongue
9. Changes in the Operation of Implanted Cardiac Pacemakers
10. Changes in Circadian Rhythms

Glaser, Z. (1971). Bibliography of reported biological phenomena ('effects') and clinical manifestations attributed to microwave and radio-frequency radiation. Navel Medical Research Institute. https://archive.org/details/DTIC_AD0750271/mode/2up?view=theater​

The study, conducted in the Fertility Clinic at Massachusetts General Hospital, is the first to examine associations between organophosphate flame retardants (PFRs)—which are used in polyurethane foam in many products, including upholstered furniture, baby products, gym mats, and even some phone cases—and reproductive outcomes in women. PFR's can be absorbed by the body through physical contact. These chemicals are not chemically bonded to foam and have been shown to migrate into the air and dust of indoor environments

“These findings suggest that exposure to PFRs may be one of many risk factors for lower reproductive success,” said first author Courtney Carignan. “They also add to the body of evidence indicating a need to reduce the use of these flame retardants and identify safer alternatives.”

Infertility, defined as the inability to get pregnant after 1 y or more of unprotected intercourse, affects one in six couples worldwide. One study found that pregnancy loss (miscarriage) affected approximately 28% of couples planning a pregnancy. Infertility has an associated health-care cost in the billions of dollars per year, not including the physical and psychological burden placed on the couple. Both the high rates of fertility along with the associated high costs should prompt the need to improve our understanding of risk factors that impair the ability to have a child.

One potential risk factor is environmental exposure. Several classes of endocrine-disrupting chemicals (EDCs) with widespread general population exposure, including pesticides and phthalates, have been linked to infertility and adverse pregnancy outcomes. Since EDCs are ubiquitous, only a fraction have been evaluated for effects on infertility and pregnancy. PFRs are a class of EDCs with omnipresent exposure that have been detected in 90–100% of adult urine samples. Over the past decade, PFRs have been used widely in the polyurethane foam of upholstered furniture as replacements for pentabromodiphenyl ether, a flame retardant mixture that was phased out of use in 2005.

Animal studies indicate that exposure to PFRs can disrupt endocrine function through altered thyroid action, steroidogenesis, or estrogen metabolism, and can also impair embryo development. Researchers have observed  increasing PFR exposures were associated with a decrease in sperm motility and increased serum total T3 levels, in a small study of men. 

The aforementioned study explored the association between urinary concentrations of PFRs and pregnancy outcomes among women in a prospective cohort study, the Environment And Reproductive Health (EARTH) study, using assisted reproductive technologies (ART) as a model to study early developmental endpoints and pregnancy outcomes.

In conclusion, using IVF (in vitro fertilization) as a model to investigate human reproduction and pregnancy outcomes, we found that concentrations of some urinary PFR metabolites were inversely associated with proportions of successful fertilization, implantation, clinical pregnancy, and live birth. These results highlight the potential reproductive effects of low-level exposure (i.e., background exposure levels of the general population) to PFRs and adverse IVF outcomes. Future research should focus on potential interactions between PFRs and other chemicals (i.e., mixtures analysis) that adversely affect reproductive health and also explore the potential effect of PFRs on male reproductive health.

The work was supported by grants ES009718, ES022955, ES000002, and T32ES007069 from the National Institute of Environmental Health Sciences (NIEHS).

According to the National Cancer Institute, the rate of new melanoma cases among American adults has tripled since the 1970s, from 7.9 per 100,000 people in 1975 to 25.2 per 100,000 in 2014 (National Cancer Institute, 2017). A similar trend can be observed in regards to melanoma death rate for white American men, the highest risk group, which has escalated sharply, from 2.6 deaths per 100,000 in 1975 to 4.4 in 2014. From 2003 to 2012, the rates of new melanoma cases among both men and women have been increased by 1.7 and 1.4 percent per year (Centers for Disease Control and Prevention, 2016).

While the exact cause of melanoma is unknown, researchers have established that risk factors for melanoma include family history, indoor tanning, the number of moles on a person’s skin, fair skin, freckles, blue or green eyes, blonde or red hair and a history of severe sunburns, among others (Centers for Disease Control and Prevention, 2017). People are able to modify only three of these risk factors: indoor tanning, exposure to UV radiation and severe sunburns.

In December 2012, the Food and Drug Administration began to enforce new laws designed to improve sunscreens and consumer protection. The new laws restrict certain bogus label claims, but they allow most sunscreens to advertise “broad spectrum” skin protection. Sunscreen manufacturers are permitted to tell consumers, that with proper use, their products can help reduce the risk of skin cancer. However, the FDA and the International Agency for Research on Cancer have concluded that the available data does not support the assertion that sunscreens alone reduce the rate of skin cancer (Food and Drug Administration, 2011; IARC 2001).

Recent research by the Center for Disease Control and Prevention found 96% of the U.S. population has oxybenzone in their bodies, a common chemical used in sunscreens; a chemical that is a known endocrine disruptor, linked to reduced sperm count in men and endometriosis in women (Environmental Working Group, 2017).

Researchers have observed that adults who put on sunscreen containing 4% oxybenzone (the US allows up to 6%) in the morning and evening—mimicking what they’d do while on vacation—continued to excrete the chemical in their urine for five days afterwards, suggesting that it was being stored in the body (Gustavsson Gonzalez, Farbrot & Larko, 2002).

Aside from oxybenzone — which is found in 70% of sunscreens — other commonly used chemicals that can enter your bloodstream and can cause toxic side effects, including hormone disruption, include but are not limited to:

Mechanical sunscreens, including zinc oxide and titanium dioxide, have proven over years of use to be safe and effective mechanisms for blocking both UVA and UVB light. According to the Environmental Working Group (EWG) - a non-profit environmental organization that specializes in research and advocacy in the areas of toxic chemicals, agricultural subsidies, public lands, and corporate accountability - sunscreens made with zinc oxide and titanium dioxide are better alternatives because they provide strong sun protection with few health concerns and they don’t break down in the sun. Zinc oxide is EWG’s first choice for sun protection. Most studies to date have shown that zinc oxide and titanium dioxide are safe and unlikely to penetrate your skin when applied topically, as long as they are not nanosized. However, in an attempt to meet the desire of their consumers for products that don't leave a thick film on the skin, some manufacturers have reduced the size of the molecules, creating nanoparticles (microscopic particles measuring less than 100 nanometers).

This nanotechnology has several different effects. Some are concerned that the particles have become so small that they may be absorbed directly into your skin. Although mixed, some studies have found significant negative health effects from the absorption of nanoparticles (European Union Public Health, 2006). While these nanoparticle technologies may make an excellent drug delivery system, it is questionable for use in sunscreen (De Jong & Borm, 2008).

Titanium dioxide is more effective in UVB range and zinc oxide in the UVA range, therefore the combination of these particles assures a broad-band UV protection (Smijs & Pavel, 2011). Zinc oxide is beneficial because it remains stable in heat, but as a nanoparticle, the problems with toxicity probably outweigh the benefits to sun protection. Upon systemic distribution, toxicity of zinc oxide nanoparticles may affect the lungs, liver, kidneys, stomach, pancreas, spleen, heart and brain (Tian et al., 2015). Findings have also demonstrated that aging has a synergistic effect with zinc oxide nanoparticles on systemic inflammation and neurotoxicity, affecting your brain and neurological system. In other words, the older you are, the higher your risk of neurotoxicity from zinc oxide nanoparticle absorption.

Spray-on sunscreens, containing zinc oxide and/or titanium dioxide, pose an additional hazard by releasing these toxic nanoparticles into the air. The FDA has previously expressed concern that inhaling these products may be risky, especially to children, and has warned parents to avoid spray-on sunscreens (Food and Drug Administration, 2006).
While these two minerals are the safest topical sunscreen agents around, inhaling them is a whole different story. When these minerals are inhaled, they have been shown to irritate lung tissues and potentially lead to serious health problems, and the finer the particles, the worse their effects appear to be (Grassian, O’Shaughnessy, Adamcakova-Dodd, Pettibone & Thorne, 2006). The lungs have difficulty clearing small particles, and the particles may pass from the lungs into the bloodstream. Insoluble nanoparticles that penetrate skin or lung tissue can cause extensive organ damage. Some researchers speculate that the toxic effects of nanoparticles relate to their size being in the range of a virus, which may trigger your body's immune response (Buzea, Pacheco Blandino & Robbie, 2007).

The International Agency for Research on Cancer (IARC) has classified titanium dioxide as a "possible carcinogen" when inhaled in high doses. According to IARC:

"Titanium dioxide causes varying degrees of inflammation and associated pulmonary effects including lung epithelial cell injury, cholesterol granulomas and fibrosis. Rodents experience stronger pulmonary effects after exposure to ultrafine titanium dioxide particles compared with fine particles on a mass basis (IARC, 2006).

The use of nanoparticles in cosmetics poses a regulatory challenge because the properties of nanoparticles may vary tremendously, depending on their size, shape, surface area and coatings. A number of manufacturers sell products advertised as containing “non-nano” zinc oxide and titanium dioxide - these claims are generally misleading. While particle sizes vary among manufacturers, nearly all would be considered nanomaterials under a broad definition of the term, including the definition proposed in 2011 by the Food and Drug Administration (Food and Drug Administration, 2011b). According to the available information, these mineral sunscreens must be delivered in nanoparticle form to render a layer that is reasonably transparent on the skin.

According to EWG, even with the existing uncertainties, zinc oxide and titanium dioxide lotions are among the best choices on the American market. Here’s why:

• The shape and size of the particles affect sun protection.

The smaller they are, the better the SPF protection and the worse the UVA protection. Manufacturers must then find a balance: small particles provide greater transparency but larger particles offer greater UVA protection. The form of zinc oxide most often used in sunscreens is larger and provides greater UVA protection than the titanium dioxide products that appear clear on the skin.

• Nanoparticles in sunscreen may not penetrate the skin.

Some studies indicate that nanoparticles can harm living cells and organs when administered in large doses. But a large number of studies have produced no evidence that zinc oxide nanoparticles can cross the skin in significant amounts. Researchers found that less than 0.01 percent of either form of zinc entered the bloodstream. The study could not determine if the zinc in the bloodstream was insoluble nanoparticles, therefore the European regulators concluded it was most likely zinc ions, which would not pose any health risk (Scientific Committee on Consumer Safety, 2012). However, more research should be conducted to reach definitive conclusions.

• It is unlikely that nanoparticles in sunscreen cause skin damage when energized by sunlight.

Titanium dioxide, and to a lesser extent zinc oxide, are photocatalysts, meaning that when they are exposed to UV radiation they can form free radicals that damage surrounding cells. Nanoparticle sizes of these minerals are more affected by UV rays than larger particles. Sunscreen manufacturers commonly employ surface coatings that can dramatically reduce the potential for photoactivity, with data suggesting that they reduce UV reactivity by as much as 99% (SCCNFP..., 2000). In sunscreens, problems may arise if particles are not treated with inert coatings, if the coatings are not stable, or if manufacturers use forms of zinc oxide or titanium dioxide that are not optimized for stability and sun protection. However, tests of living skin from human volunteers and animal testing suggest that these hazards are not a concern for human safety because the free radicals that are generated by nanoparticles on skin are quenched by the skin’s own antioxidant protections (Popov et al., 2009).

Currently, all available evidence suggests that zinc oxide and titanium dioxide can be safely used in sunscreen lotions applied to healthy skin and pose a lower hazard than most other approved sunscreen ingredients.

More human studies need to be conducted in regards to the health effects of inhaling of zinc oxide particles, especially at lower levels, such as from brief exposure to sunscreen spray. However, using these spray-on products are clearly an unnecessary risk since safer options are readily available. Your safest bet is to use topical zinc oxide or titanium dioxide that does not contain nanosized particles.

In theory, applying sunscreen with a sun protection factor (SPF) of 100 would allow sunbathers to be exposed to the sun 100 times longer before suffering a sunburn. For example, an individual who would normally redden after 30 minutes in the afternoon sun could theoretically stay out for 50 hours.

But for high-SPF sunscreens, theory and reality are two different things. Researchers have observed that people are misled by the claims on high-SPF sunscreen bottles. They are more likely to use high-SPF products improperly and as a result may expose themselves to more harmful ultraviolet radiation than people relying on products with lower SPF values. The FDA has long contended that SPF higher than 50 is “inherently misleading” (Food and Drug Administration, 2007).

Here are some reasons against applying sunscreens with SPF values greater than 50:

• Marginally better sunburn protection.

Sunbathers often assume that they get twice as much protection from SPF 100 sunscreen as from SPF 50. In reality, the extra protection is negligible. Properly applied SPF 50 sunscreen blocks 98% of UVB rays, while SPF 100 blocks 99%. When used correctly, sunscreen with SPF values in the range of 30 to 50 will offer adequate sunburn protection, even for people most sensitive to sunburn.

• Consumers misuse high-SPF products.

High-SPF products tend to deceive users into staying in the sun longer and overexposing themselves to both UVA and UVB rays. Saturated with a false sense of security, people extend their time in the sun well past the point when users of low-SPF products would head indoors. As a result, they get as many UVB-inflicted sunburns as unprotected sunbathers and are likely to absorb more damaging UVA radiation.

Researchers have conducted numerous studies on sunbathers and have observed that high-SPF products spur “profound changes in sun behavior” that may account for the increased melanoma risk found in some studies. The researchers confirmed that European vacationers spent more total time in the sun if they were given an SPF 30 sunscreen instead of an SPF 10 product (Autier et al., 2000). It is assumed the difference would also apply to products with SPF values greater than 50.

Here are some helpful tips to help protect yourself from the sun's harmful UV rays:

Your safest and best choice for sunscreen protection is zinc oxide. However, avoid nanoparticles, which are common in spray sunscreens, to circumvent potential toxicity. Unfortunately, it can be challenging to find a product without other chemical additives. To help you choose the safest product, EWG performs an annual sunscreen evaluation based on effectiveness and safety.

Ambati, R., Moi, P., Ravi, S., & Aswathanarayana, R. (2014). Astaxanthin: Sources, Extraction, Stability, Biological Activities and Its Commercial Applications—A Review. Marine Drugs, 12(1), 128-152. http://dx.doi.org/10.3390/md12010128

Autier, P., Doré, J.-F., Reis, A. C., Grivegnée, A., Ollivaud, L., Truchetet, F., … Césarini, J.-P. (2000). Sunscreen use and intentional exposure to ultraviolet A and B radiation: a double blind randomized trial using personal dosimeters. British Journal of Cancer, 83(9), 1243–1248. http://doi.org/10.1054/bjoc.2000.1429

Buzea, C., Pacheco Blandino, I., & Robbie, K. (2007). Nanomaterials and nanoparticles: Sources and toxicity. Biointerphases. Retrieved 3 August 2017, from https://arxiv.org/ftp/arxiv/papers/0801/0801.3280.pdf

Centers for Disease Control and Prevention. (2017). What Are the Risk Factors for Skin Cancer?. Cdc.gov. Retrieved 3 August 2017, from https://www.cdc.gov/cancer/skin/basic_info/risk_factors.htm

Centers for Disease Control and Prevention. (2016). Skin Cancer Trends. (2017). Cdc.gov. Retrieved 3 August 2017, from https://www.cdc.gov/cancer/skin/statistics/trends.htm

De Jong, W. H., & Borm, P. J. (2008). Drug delivery and nanoparticles: Applications and hazards. International Journal of Nanomedicine, 3(2), 133–149.

Environmental Working Group. (2017). EWG's 2017 Guide to Safer Sunscreens. Ewg.org. Retrieved 3 August 2017, from http://www.ewg.org/sunscreen/report/the-trouble-with-sunscreen-chemicals/#.WYKSS4UnHPp

European Union Public Health. (2006). What are potential harmful effects of nanoparticles?. Ec.europa.eu. Retrieved 3 August 2017, from http://ec.europa.eu/health/scientific_committees/opinions_layman/en/nanotechnologies/l-3/6-health-effects-nanoparticles.htm

Food and Drug Administration. (2011). Labeling and Effectiveness Testing: Sunscreen Drug Products for Over-the-Counter Human Use. Regulations.gov. Retrieved 3 August 2017, from https://www.regulations.gov/document?D=FDA-1978-N-0018-0698

Food and Drug Administration. (2011b). FDA Draft, Not for Implementation: Guidance for Industry. Enforcement Policy – OTC Sunscreen Drug Products Marketed Without an Approved Application. Available at www.fda.gov/downloads/Drugs/GuidanceComplianceRegulatoryInformation/Guidances/UCM259001.pdf

Food and Drug Administration. (2006). PETITION REQUESTING FDA AMEND ITS REGULATIONS FOR PRODUCTS COMPOSED OF ENGINEERED NANOPARTICLES GENERALLY AND SUNSCREEN DRUG PRODUCTS COMPOSED OF ENGINEERED NANOPARTICLES SPECIFICALLY. FDA.gov. Retrieved 3 August 2017, from https://www.fda.gov/ohrms/dockets/dockets/06p0210/06p-0210-cp00001-01-vol1.pdf

Food and Drug Administration. (2007). Sunscreen Drug Products for Over-the-Counter Human Use; Proposed Amendment of Final Monograph; Proposed Rule - FR Doc 07-4131. (2017). Fda.gov. Retrieved 3 August 2017, from https://www.fda.gov/OHRMS/DOCKETS/98fr/07-4131.htm

Grassian, V., O’Shaughnessy, P., Adamcakova-Dodd, A., Pettibone, J., & Thorne, P. (2006). Inhalation Exposure Study of Titanium Dioxide Nanoparticles with a Primary Particle Size of 2 to 5 nm. Environmental Health Perspectives, 115(3), 397-402. http://dx.doi.org/10.1289/ehp.9469

Gustavsson Gonzalez, H., Farbrot, A., & Larko, O. (2002). Percutaneous absorption of benzophenone-3, a common component of topical sunscreens. Clinical And Experimental Dermatology, 27(8), 691-694. http://dx.doi.org/10.1046/j.1365-2230.2002.01095.x

International Agency for Research on Cancer (IARC). (2006). IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. IARC.fr. Retrieved 3 August 2017, from https://monographs.iarc.fr/ENG/Monographs/vol93/mono93.pdf

IARC. (2001). IARC Summary Recommendations for Public Health Action. IARC. Retrieved 3 August 2017, from http://www.who.int/uv/resources/recommendations/en/IARCSum.pdf

Mercola, J. (2017). Is Your Sunscreen Doing More Harm Than Good?. Mercola.com. Retrieved 3 August 2017, from http://articles.mercola.com/sites/articles/archive/2017/04/26/hazardous-chemicals-in-sunscreens.aspx

National Cancer Institute. (2017). Melanoma of the Skin - Cancer Stat Facts. Seer.cancer.gov. Retrieved 3 August 2017, from http://seer.cancer.gov/statfacts/html/melan.html

National Toxicology Program (NTP). (2000). Broad-Spectrum Ultraviolet (UV) Radiation and UVA, and UVB, and UVC. U.S. Department of Health and Human Services. Retrieved 3 August 2017, from https://ntp.niehs.nih.gov/ntp/newhomeroc/roc10/uv_no_appendices_508.pdf

NTP Technical Report on the Photococarcinogenesis Study of Retinoic Acid and Retinyl Palmitate [CAS Nos. 302-79-4 (All-Trans-Retinoic Acid) and 79-81-2 (All-Trans-Retinyl Palmitate)] in SKH-1 Mice (Simulated Solar Light And Topical Application Study). NTP TR 568, National Institutes of Health, 2012. Available at ntp.niehs.nih.gov/ntp/htdocs/LT_rpts/TR568_508.pdf

Popov, A., Haag, S., Meinke, M., Lademann, J., Priezzhev, A., & Myllylä, R. (2009). Effect of size of TiO[sub 2] nanoparticles applied onto glass slide and porcine skin on generation of free radicals under ultraviolet irradiation. Journal Of Biomedical Optics, 14(2), 021011. http://dx.doi.org/10.1117/1.3078802

SCCNFP, Opinion Concerning Titanium Dioxide. Opinion: European Commission – The Scientific Committee on Cosmetic Products and Non-Food Products Intended for Consumers. (2000). Retrieved 3 August 2017, from http://ec.europa.eu/health/ph_risk/committees/sccp/documents/out135_en.pdf

Scientific Committee on Consumer Safety. (2012). Opinion on Zinc oxide (nano form).  Retrieved 3 August 2017, from http://ec.europa.eu/health/scientific_committees/consumer_safety/docs/sccs_o_103.pdf

Smijs, T. G., & Pavel, S. (2011). Titanium dioxide and zinc oxide nanoparticles in sunscreens: focus on their safety and effectiveness. Nanotechnology, Science and Applications, 4, 95–112. http://doi.org/10.2147/NSA.S19419

Tian, L., Lin, B., Wu, L., Li, K., Liu, H., & Yan, J. et al. (2015). Neurotoxicity induced by zinc oxide nanoparticles: age-related differences and interaction. Scientific Reports, 5(1). http://dx.doi.org/10.1038/srep16117