To live in the 21st century is to live in a toxic world. Our increased exposure to pollutants such as carbon dioxide, volatile organic compounds, and endocrine-disrupting chemicals increases the risk of many chronic illnesses such as cancer, heart disease, and lung disease. Read more to learn about the detrimental effects of pollution and environmental toxins on human health.
Following the industrial revolution, the increased urbanization and economic development have led to a surge in energy consumption and waste emissions .
Because of this, environmental pollution is reaching troubling proportions worldwide. According to a recent World Health Organization (WHO) report, 92% of the world’s population are living in polluted regions that exceed WHO safety limits .
Children in these areas are especially at risk. A UNICEF report (October 2016) found that nearly 600,000 children under age five die annually from diseases caused or exacerbated by outdoor and indoor air pollution, particularly in lower-income countries .
The alarming rise in environmental pollutants is considered a major public health problem, costing the United States nearly $340 billion in annual healthcare expenditures and lost productivity .
Among the most concerning of these pollutants are carbon monoxide (CO), sulfur dioxide (SO2), nitrogen oxides (NOx), volatile organic compounds (VOCs), ozone (O3), heavy metals, and respirable particulate matter, all of which have been linked to prenatal defects, respiratory disorders, heart disease, and mental disorders, as well as increased likelihood of disease and reduced life expectancy [2, 1].
Many of these chemicals originate from man-made sources including transportation sources (e.g., vehicles), stationary sources (e.g., factories, power plants, and refineries), and indoor sources (e.g., building, cleaning, and cooking materials) [5, 6].
The following conditions have been associated with exposure to pollution. Note, however, that the majority of studies covered in this section deal with associations only, which means that a cause-and-effect relationship hasn’t been established. Additionally, some of them are complex disorders that involve many other possible factors that may vary from one person to another.
Particulate matter (PM), a major component of outdoor air pollution, is classified as a group 1 carcinogen by the International Agency for Research on Cancer (IARC), meaning that there is enough evidence to conclude that it causes cancer in humans [7, 8].
Cancer rates are skyrocketing in villages across China (where the levels of air pollution are among the highest observed worldwide), a phenomenon credited to rising levels of atmospheric particulate matter from the exhaust, coal smoke, and vehicle fumes in these regions .
The International Agency for Research on Cancer and multiple meta-analyses also found that long-term air pollution exposure is a direct cause of lung cancer. Lung tissues are particularly susceptible because of their extensive contact with inhaled airborne carcinogens [9, 10, 11].
Volatile organic compounds are organic compounds that can become volatile (gaseous) at room temperatures. They are found at higher levels indoors due to their emission by many common household products and office materials (e.g., paints, carpets, air fresheners, disinfectants, and pesticides) [12, 13, 14].
A number of volatile organic compounds are suspected or known to cause cancer, including benzene, formaldehyde, vinyl chloride, carbon tetrachloride, 1,2-dichloroethane, trichloroethylene, and chloroform. Chronic exposures have been linked to the development of leukemia, lymphoma, myeloma and angiosarcoma in humans [15, 16, 17, 18].
In the World Health Organization’s (WHO) Global Burden of Disease project, it was estimated that urban air pollution worldwide (as measured by concentrations of PM) contributes to about 5% of all deaths from tracheal, bronchial, and lung cancers .
The main evidence of the carcinogenic mechanisms of air pollution comes from human and animal biomolecular studies revealing its association with DNA damage, inflammation, oxidative stress, altered telomere length, and impaired DNA methylation .
Epidemiological studies indicate that air pollution is correlated with an increased frequency of respiratory allergy, especially in people living in urban areas compared to rural populations .
Subsets of particulate matter smaller than a certain size (≤0.1 μm), known as PM0.1, are particularly dangerous. These particles can penetrate the deepest (alveolar) portions of the lung and enter the blood circulation, causing direct damage to a variety of different organ tissues .
Children growing up in heavily polluted areas (with high O3, PM, and aldehyde levels) exhibit irregular structural changes in the nasal lining. These defects can lead to impaired airway clearance, lung infection and inflammation [22, 23, 24, 25].
High levels of ozone are associated with extensive airway and lung tissue damage as well as more severe asthma symptoms and increased respiratory hospital admissions/deaths in Europe and the US [27, 28].
Other components of traffic-related pollution such as sulfur oxides, nitrogen oxides, and carbon monoxide have been linked to the development of respiratory complications including lung congestion, fluid build-up in lung tissues, wheezing, and lung infections [29, 30, 31, 32].
In a study of middle-aged and older adults, a minimal (2 µg) increase in PM was associated with a higher risk of brain stroke and smaller brain volume, both biomarkers of brain aging. Two meta-analyses associated the exposure to PM subsets smaller than 2.5 µm (PM2.5) and 10 µm (PM10) with an increased incidence of stroke and death rate from this condition [36, 37, 38].
A meta-analysis also associated PM2.5 with an increased incidence of neurological disorders such as dementia, Alzheimer’s disease, autistic spectrum disorders, and Parkinson’s disease .
Carbon dioxide and volatile organic compounds, both commonly found in new buildings, are believed to be related to sick building syndrome, a condition characterized by headaches, memory problems, drowsiness, and mental confusion/“brain fog”.
A clinical trial found that the cognitive performance (i.e., crisis response, strategy, and information usage) of office people who worked in conditions with low carbon dioxide and volatile organic compound levels was nearly twice better than that of those who worked in conventional office environments (with high volatile organic compounds and carbon dioxide), indicating that these chemicals can diminish intellectual capacity .
NO2, for which motorized traffic is a major source, was associated with delayed psychomotor development in children born to highly exposed mothers .
Despite the increased use of unleaded gasoline, lead still remains an outdoor air pollutant in many parts of the world. Prenatal exposures have been shown to alter brain function and lower IQ levels in children. Similarly, occupational exposure in adults was associated with a reduced neurocognitive performance [42, 43].
Inhaling other heavy metals can cause neurobehavioral impairments .
For example, mercury, an element released from coal-burning power plants, is toxic to brain cells and can lead to a neurological disorder characterized by irritability, difficulty concentrating, cognitive impairment and memory loss (erethism) .
High-level exposures to manganese can also cause neurological defects. One study found that Mn concentration (in blood, urine, and toenail samples) was inversely correlated with overall neurocognitive performance (assessed by memory, concentration, and motor tests) in welders and smelters .
Exposure to cadmium during pregnancy was associated with an impaired cognitive development of the offspring, especially regarding language, performance ability, and general cognitive development .
The most concerning of these air-borne pollutants include carbon monoxide, nitrogen oxide, sulfur dioxide, ozone, lead, and particulate matter. These pollutants are associated with high rates of hospitalization and death due to heart disease, especially in patients with congestive heart failure and abnormal heart rate (arrhythmia ) .
A meta-analysis associated exercising in polluted environments with higher blood pressure and impaired blood vessel function, both of which are risk factors for heart disease .
This is likely due to the promotion of vascular dysfunction, inflammation, oxidative stress, blood clot formation, and increased blood pressure by pollutants, all of which are risk factors for heart disease/failure .
Also, some pollutants (e.g., ozone and PM) can stimulate lung nerve reflexes and increase fight-or-flight (sympathetic) stimulation, resulting in irregular heart rate and reduced variability [55, 56].
High concentrations of particulate matter (PM2.5) impaired energy metabolism and glucose homeostasis, in addition to increasing inflammation in insulin-responsive organs, in an animal model of type 2 diabetes and have been associated with this condition in humans after long-term exposure [60, 61].
Chronic exposure to air pollution can also worsen the clinical outcomes of diabetic patients. One study showed that pollutant exposure enhanced the vulnerability of diabetic patients to heart disease and stroke risk factors .
Although genetic factors are implicated in autoimmune disease, the incidence of autoimmunity is rising too rapidly to conclude that only population-level genetic changes are responsible, indicating that environmental factors are largely involved .
Indeed, many people with environmental illnesses have an array of autoimmune diseases linked to air pollution .
Organic solvent exposure is a risk factor for autoimmune disease and has been associated with the development of systemic sclerosis, primary systemic vasculitis, and multiple sclerosis in humans .
Studies in brain cell cultures showed that diesel exhaust particles can activate microglia and induce the death of dopaminergic neurons (by increasing inflammation and reactive oxygen species). Because dopamine depletion in the brain is involved in the development of depression, air pollution may trigger or exacerbate depressive symptoms by inducing dopaminergic neurotoxicity [69, 70].
Data from human observational studies support an association between air pollution (e.g., CO, NO2, O3, PM) and frequency of depressive disorders, suicide attempts, and even migraine and headache symptoms [71, 72, 73].
Organic solvents (e.g., toluene, xylene, benzene, and trichloroethylene) have been reported to cause a number of psychological/mood disturbances including anxiety, depression, and panic attacks in exposed individuals .
Airborne particle exposure is strongly associated with skin aging signs, particularly pigment spots and wrinkles .
Eczema and hives are more common in city dwellers (where there is a high amount of pollution) compared to people living in rural areas. Particulate matters (PM2.5 and PM10) are especially associated with eczema and other skin conditions [76, 77, 78].
The damages possibly stem from the ability of many pollutants to pass through the skin and activate inflammatory pathways, stimulate melanin production from melanocytes (causing unwanted sunspots), and trigger new blood vessel growth (causing redness and Rosacea) .
There is an alarming rise in spontaneous abortions among wildlife species across the U.S., which scientists are attributing to environmental pollutant exposure .
Similarly, a marked reduction in live birth rates and increased risk of miscarriage was observed in women undergoing in vitro fertilization and exposed to high concentrations of nitrogen dioxide and particulate matter [81, 82].
A number of these pollutants are hormonal disruptors and can interfere with the action of hormones that control growth, development, and fertility .
Studies have shown that these chemicals tamper with estrogen, androgen, and progesterone receptors, leading to a myriad of reproductive anomalies in humans and animals (i.e., preterm birth, miscarriage, birth defects, low sperm count, and prostate cancer) [84, 85].
Air pollution also has a negative impact on semen quality. Several studies in men found that high-level air pollution exposure was significantly associated with defects in a number of semen measures including fewer motile sperm, more abnormally-shaped sperm and more sperm chromosomal aberrations [86, 87, 88].
Extracts of outdoor and indoor airborne particulate matter significantly inhibit thyroxine (T4) binding to transthyretin, a carrier protein that transports this hormone throughout the body. Transthyretin binding inhibition can lead to blood thyroid hormone depletion, which disrupts thyroid homeostasis and potentially increases the risk of thyroid cancer [91, 92].
Pollutants from car emissions and organic solvents are believed to trigger autoimmune thyroid diseases by interfering with iodine transportation and inducing oxidative stress, thereby initiating an inflammatory response to the thyroid gland .
Some pollutants act as hormonal disruptors (e.g., PCBs, BPAs, and phthalates) and block thyroid hormone binding to its receptor.
Elevated levels of traffic-related pollution are associated with a higher body mass index in children .
Air pollutants have been proposed to trigger inflammatory pathways that promote diabetes and fat storage. This theory is supported by animal studies showing that mice exposed to air pollution and fed a fat chow diet developed more body fat and insulin resistance than those eating the same diet but breathing clean air .
This is attributed to the stimulated production of reactive oxygen species (ROS) and inflammatory markers by pollutants, which damages telomeric DNA and accelerates the rate of its attrition [100, 101].
Progressive telomere shortening leads to cellular aging, death, or transformation into cancerous cells, thereby elevating the risk of many chronic conditions including cancer and heart disease .
An observational study in Taiwan found that carbon monoxide and nitrogen dioxide exposure was associated with an increased risk of osteoporosis in men and women .
Air pollution exposure induces systemic and tissue-specific inflammation, which may decrease bone mineral density by stimulating bone loss (osteoclastic) activity. This idea is further supported by studies revealing bone mineral density loss in patients with chronic inflammatory diseases [103, 104].
Fluorine, an element commonly used in many industrial processes, can build up in bones (during chronic high-level exposures) and cause hypermineralization (hardening of bone). This may result in reduced joint mobility, abnormal bone formation, and an increased risk of bone fractures [105, 106, 107].
Long-term exposures can also lead to dental fluorosis, a condition manifested by white, yellow, brown, and black stains on tooth enamel .
Because the kidneys receive roughly 25% of the resting heart output (despite making up only about 0.5% of total body mass), large amounts of chemicals and drugs in the body circulation are delivered to the kidneys .
Also, as kidneys form concentrated urine, they accumulate toxic pollutants in the tubular fluid. Thus, a pollutant present at nontoxic levels in the blood can reach toxic levels in the kidney, increasing the likelihood of tissue injury .
One study in China found higher rates of membranous nephropathy, an immune disorder that can lead to kidney failure, in regions with elevated levels of fine PM .
Air pollutants such as diesel exhaust particles, particulate matter, coal fly ash, and carbon black have been shown to induce liver toxicity and worsen liver inflammation and fat build-up in several animal models, suggesting that they may trigger or exacerbate liver diseases in humans .
A meta-analysis of 5 studies on almost 300 petrochemical plant workers found an association between exposure to petrochemicals and increased incidence of fatty liver disease and liver damage .
Residents living in heavily polluted areas are at higher risk of developing dry eye syndrome .
Age-related cataracts are a leading cause of blindness worldwide. Smoking, a major source of indoor pollution, is strongly linked to cataract formation, likely due to the presence of cadmium and lead in cigarette smoke .
Evidence from animal models suggests that chronic gut exposure to high levels of particulate matter could lead to the development of GI inflammatory diseases by increasing gut permeability, decreasing colonic motility, and altering gut microbiota composition and function [117, 118].
- Purifying indoor air: Air cleaning systems can reduce indoor pollutant levels of outdoor/indoor origin. You need to make sure to get systems that can purify VOCs and gases.
- Staying indoors (assuming you have a purifier): Environmental protection agencies in many countries advise people to stay indoors during days with high amounts of air pollution. However, some outdoor pollutants such as PM, ozone, and other gasses can infiltrate indoors, with infiltration rates varying due to differences in building structures and operating conditions. Levels of indoor air pollutants of outdoor origin are mainly determined by the means of outdoor-to-indoor transport, which is dependent on the air exchange rate. Closing windows can effectively reduce the air exchange rate (up to 50%) and reduce outdoor pollutant infiltration.
- Avoiding outdoor activity when levels are high: Avoiding rigorous, extended outdoor activity during high air pollution days and/or near high-traffic roadways and sources of combustion (e.g., wood burning) reduces pollutant inhalation.
- Quitting smoking: Environmental tobacco smoke (ETS) or secondhand smoke is a major source of indoor air pollution and a significant contributor to indoor PM and VOC levels.
- Opting for safer consumer products: Many commercial products are key sources of indoor air pollutants including VOCs and endocrine-disrupting compounds (e.g., pesticides, polybrominated diphenyl ethers, flame retardants, polychlorinated biphenyls, alkylphenols, surfactants, and parabens). Reading labels and choosing products that are mainly plant-based, paraben-free, fragrance-free, and that do not contain ethanolamines organochlorines, antimicrobials (e.g. triclosan), alkylphenol-based surfactants (i.e. nonionic surfactants), dichlorobenzene, phthalates, methylene chloride, toluene, and carbon tetrachloride can limit indoor exposure to these chemicals
If you want to eliminate the pollutants that build up in your body and reduce their damage, you may try the following complementary approaches if your doctor determines that they may be helpful in your case.
Many studies have highlighted the impact of micronutrients/supplements in mitigating the harmful effects of air pollution. Research shows that:
- Airway hyperresponsiveness induced by NO2 was completely prevented with vitamin C pretreatment in a clinical trial on 11 people .
- Vitamin C, vitamin E, and beta-carotene may protect against the short-term effects of high ozone exposure on lung functions and alleviate nasal inflammation 
- Broccoli/broccoli sprouts rich in glucoraphanin reduced the harmful impact of PM pollution on allergic diseases and asthma in a clinical trial on 29 people .
- Polyunsaturated fatty acids (PUFAs) and vitamin E can reduce lung inflammation and oxidative stress induced by PM2.5 .
- Vitamin C and E supplementation can reduce fat/protein/ DNA damage by boosting antioxidant defenses .
- PUFAs and B vitamins can improve heart function and prevent heart rate variability (HRV) decline induced by PM2.5 .
Additionally, NRF2 is a major activator of pathways that reduce oxidative damage with a proven role in protecting from respiratory disorders, as well as heart disease associated with particulate matter. You can take NRF2 supplements or read here how to activate it [127, 128].
However, remember that none of these substances is approved for medical use by the FDA. Supplements generally lack solid clinical research. Regulations set manufacturing standards for them but don’t guarantee that they’re safe or effective. Speak with your doctor before supplementing and never use them as a replacement for proven therapies.