“We haven’t experienced a full night’s sleep since our son was born eight years ago,” Mrs. B mentioned, referring to her son’s dry, red, and itchy skin. Her son has suffered from eczema throughout his life. Known as atopic dermatitis, this chronic skin ailment affects roughly 1 in 5 children in industrialized countries. Some studies suggest that the incidence of eczema in developing countries is significantly lower, more than thirty times less, compared to developed nations. However, the rise in eczema cases didn’t occur during the Industrial Revolution, which began around 1760. Instead, countries like the U.S., Finland, and others witnessed a sharp increase in eczema cases around 1970. What triggered this surge in eczema cases? I am an allergist and immunologist, and my colleagues and I are investigating trends in eczema rates in the U.S. It is understood that factors like diets high in processed foods and exposure to certain detergents and chemicals can heighten the risk of developing eczema.
Proximity to factories, major roadways, or wildfires increases the likelihood of developing eczema. Environmental exposures can also originate indoors, such as from paint, plastics, cigarette smoke, or synthetic fabrics like spandex, nylon, and polyester. Although a lot of research focuses on genetics, environmental factors during a child’s early years are the best indicators of whether they will develop eczema. To understand what environmental changes might have caused a spike in eczema in the U.S., we started by identifying potential hotspots, areas with eczema rates significantly above the national average. We then examined data from the U.S. Environmental Protection Agency to identify prevalent chemicals in those regions. For eczema and the allergic diseases frequently associated with it, like peanut allergy and asthma, two chemical classes stood out: diisocyanates and xylene. Diisocyanates began being produced in the U.S. around 1970 for use in spandex, non-latex foam, paint, and polyurethane manufacturing. The production of xylene also rose during this period alongside an increase in the manufacture of polyester and other materials. Diisocyanates and xylene-induced chemicals are present in cigarette smoke and wildfires as well.
In 1975, after new technology was introduced to cars to convert exhaust gases into less toxic compounds, isocyanates and xylene became part of automobile exhaust. Studies have demonstrated that exposing mice to isocyanates and xylene can cause eczema, itching, and inflammation by enhancing the activity of receptors involved in sensations of itch, pain, and temperature. These receptors also show increased activity in mice fed unhealthy diets. It’s still not known how direct exposure effects in mice compare to typical human exposure levels. How might these chemicals relate to increased eczema rates? Every person has millions of microorganisms on their skin, collectively called the skin microbiome. Although researchers don’t fully understand how beneficial bacteria support the skin, we do acknowledge their necessity in producing certain lipids or oils that seal the skin and prevent infection.
Many moisturizers and skin products contain ceramides, a lipid group crucial for skin protection. The ceramide levels on a child’s skin in their early weeks are significant predictors of future eczema. Fewer ceramides correlate with a higher likelihood of developing eczema. To identify toxins that might hinder the production of beneficial lipids that ward off eczema, my team used skin bacteria as indicators. In our lab, we exposed bacteria that directly produce ceramides, like Roseomonas mucosa, bacteria that facilitate the body’s own ceramide production, such as Staphylococcus epidermidis, and bacteria that produce other beneficial lipids, like Staphylococcus cohnii, to isocyanates and xylene. We ensured these bacteria were exposed to chemical levels typical of everyday exposure, such as standard emissions from a factory or fumes from polyurethane glue at a hardware store. We discovered that exposure to isocyanates or xylene caused these bacteria to stop producing ceramides and instead produce amino acids such as lysine. While lysine helps the bacteria mitigate the toxins’ effects, it doesn’t offer the health benefits of ceramides. We also assessed how bed sheets manufactured with isocyanates or xylene affect skin bacteria.
Harmful bacteria like Staphylococcus aureus thrived on nylon, spandex, and polyester, but couldn’t survive on cotton or bamboo. Bacteria beneficial for the skin could live on any fabric, but, similar to air pollution exposure, their beneficial lipid production dropped by more than half on synthetic fabrics compared to fabrics like cotton. What can be done about the link between pollution and eczema? Detectors that can sense low levels of isocyanate or xylene could help monitor pollutants and predict eczema flare-ups within a community. Improved detectors can also aid researchers in identifying air filtration systems capable of removing these chemicals from the environment. In the U.S., individuals can use the EPA Toxics Tracker to discover common pollutants near their homes.
Meanwhile, maintaining a balanced microbial environment may involve avoiding products that hinder the growth of healthy skin bacteria. This may mean steering clear of certain skincare products, detergents, and cleansers. Especially for children under four, avoiding cigarette smoke, synthetic fabrics, non-latex foams, polyurethanes, and some paints could be wise. Reintroducing bacteria that have been overly exposed to these chemicals might also help. For instance, my research has shown that applying Roseomonas mucosa, a ceramide-producing bacterium found on healthy skin, can result in a months-long reduction in typical eczema symptoms compared to a placebo. Other potential probiotic treatments for eczema are currently under investigation by researchers.