Prenatal exposures to environmental pollutants may lead to chronic diseases later in life.
Toxic effects of environmental pollution on human health are well recognized. Yet, for a long time conventional wisdom held that a child developing in the womb is sufficiently protected and insulated by the placenta from harmful pollutants outside. This expectation no longer holds – we know now that the developing fetus is exposed to hundreds of industrial pollutants that find their way from the mother’s body across the placenta, into the umbilical cord blood and then into the growing body of the child, as demonstrated by the ground-breaking research conducted by EWG in 2005.
Researchers worldwide are working towards understanding the full spectrum of health consequences of the prenatal, transplacental exposure to chemical pollutants. Animal studies suggest that these effects can be dramatic. For example, if a female rat is transiently exposed during the gestation period to a common vineyard fungicide vinclozolin or insecticide methoxychlor, both known endocrine disruptors, the male offspring grows up having lower sperm counts and frequent infertility. This study was carried out by scientists from the Center for Reproductive Biology at Washington State University, who noted that adverse changes in the reproductive system of male pups were associated with chemical modification of DNA structure, called DNA methylation where small chemical side chains or methyl groups are added to the primary DNA sequence.
Such changed in DNA are considered “epi-genetic” – above and beyond the straightforward DNA sequence that codes for specific genes. Epigenetics can be described as environmental instructions for the genome. Human genome contains the stored genetic information with approximately 25,000 genes packed up in chromosomes. In every cell, individual genes are turned on and off according to the functional needs of the cell. While every cell in the body has the same genome, scientists describe multiple “epigenomes,” patterns of gene activation that tells cells what they are and what they do and whether they should act as a skin cell or a heart cell.
How do epigenomes work? Twins have identical DNA, but we all know that identical twins can look very different from each other, particularly as they age – it’s their epigenetic profile that drives these differences. In a sense, DNA is like the hardware of a computer. The epigenetic profile is the software, telling the computer when and how to do its work. As we live our lives, everyone writes their own evolving software – by what they do, breathe, eat, etc. This software takes the form of methylation tags attached to the top of genes that turn genes on and off. Each tag is like a command in a computer program. Some tags are heritable, some we can change throughout life.
‘In utero’ or early life exposures to dietary and environmental exposures can have a profound effect on our epigenetic code, potentially resulting in diseases later in life, including the speed of aging and the risk of developing respiratory illness, heart disease, neurodegenerative disease, cancer, as well as behavioral and cognitive illnesses. Epigenetic changes in DNA of reproductive cells (germ line) are heritable and pass from parents to offspring. In the vinclozolin study, DNA methylation changes were passed through the germ line, so that the effects were observed in four subsequent generations examined by the scientists. In addition to reproductive problems, adult animals developed a number of diseases including prostate disease, kidney disease, high lipid levels, immune system abnormalities, testis abnormalities, and breast tumor development.
Are these findings relevant to human health? In a first-of-its-kind study published this week, researchers from the University of Cincinnati and Columbia University, NY reported that traffic pollution causes genetic changes in the womb that increase a child’s risk of developing asthma. The culprit is prenatal exposure to polycyclic aromatic hydrocarbons (PAHs), which are created as byproducts of incomplete combustion of carbon-containing fuels such as gasoline. When a mother is exposed to PAHs during pregnancy, methylation of specific genes is affected in the developing fetus which is associated with four times greater incidence of asthma symptoms in children prior to age 5. PAH levels are high in the air in heavy-traffic areas, posing health risk for inner-city neighborhoods and residential communities in proximity to major highways.
University of Cincinnati press release quoted the lead author of the study, Dr. Shuk-mei Ho: “Our data support the concept that environmental exposure can interact with genes during key developmental periods to trigger disease onset later in life, and that tissues are being reprogrammed to become abnormal later.”
The main message of the study is that we need to act quickly and decisively to protect the health of our children from toxic environmental exposures. Increased frequency of childhood diseases, such as sky-rocketing rates of asthma among children, are clearly associated with chemical pollution of the environment that acts through epigenetic mechanisms, posing a risk to the present and future human generations. Protecting our air and water from pollution and ensuring that consumer products are made without toxic chemicals will go a long way towards solving this problem. Read more
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