Body Burden: The Pollution in Newborns: Human health problems on the rise
Sources: Yeargin-Allsopp et al. 2003, CDC 1995, Robison et al. 1995, Schecter 1999, Ananth et al. 2001, Branum and Schoendorf 2002, Swan et al. 1998, Paulozzi et al. 1997, Dunson et al. 2004, Trasande and Landrigan 2004, Jahnke et al. 2005
Over the past 50 years, as infectious childhood diseases like polio, smallpox, rheumatic fever, and diphtheria have largely been controlled, chronic conditions of less obvious origins have taken their place. Asthma, autism, attention deficit and hyperactivity disorders (ADD and ADHD), childhood brain cancer and acute lymphocytic leukemia have all increased over the past 30 years. Five to ten percent of American couples are infertile. Up to half of all pregnancies end in miscarriage. Three to five percent of babies are born with birth defects (CDC 2004, Jahnke et al. 2005, Trasande and Landrigan 2004). Scientists cannot fully explain these increases, but early life exposure to environmental pollutants is a leading suspect.
Fetal exposures lead to adult disease. Some chemicals are directly toxic to an exposed child — lead and mercury, for example, which harm a developing brain — while other chemicals induce a chain of events that may culminate in a diagnosed health problem later in life. Hormone-mimicing chemicals like dioxins and furans, for example, could induce delayed cancers in hormone-sensitive tissues like the breast, testicle, or prostate gland. Chemicals like PCBs or DDT can reduce growth rates in the womb, initiating in low birthweight babies lasting, internal survival mechanisms that cascade into cardiovascular disease or diabetes later in life.
The fact is, a child can bear a lifelong imprint of risks from the countless molecules of industrial pollutants that find their way through the placenta, down the umbilical cord, and into the baby’s body. The consequences — health disorders, subtle or serious — can surface not only in childhood but also in adulthood. Studies now support origins in early life exposures for a startling array of adult diseases, including Alzheimers, mental disorders, heart disease, and diabetes.
Laboratory studies show increased deposits of the Alzheimer-related protein amyloid in the brains of older animals exposed to lead as newborns, but not in animals that were exposed to an equal amount of lead as adults (Basha et al. 2005). And over the past two decades numerous studies have linked low birth weight with adult onset of coronary heart disease, diabetes, stroke, hypertension, depression and other conditions (Barker 1995, Wahlbeck et al. 2001, Thompson et al. 2001, Hales et al. 1991). Low birth weight can arise not only from poor maternal nutrition but also from a host of industrial pollutants, including arsenic, mercury, lead, organic solvents, PCBs, and pesticides, including DDT.
Recent studies shed new light on how early life chemical exposures set adult disease in motion. In laboratory studies scientists from the University of Texas found that fetal exposures to the synthetic hormone (and now-banned drug) DES permanently “reprogrammed” body tissues, dramatically raising rates of uterine cancer, in this case, in later life (Cook et al. 2005). With an estimated 75,000 chemicals registered for use in the U.S., and an average of seven new chemicals approved each day, many not tested for safety and certaintly not tested for their ability to “reprogram” body tissues, the ramifications of this study are enormous.
Fetal exposures cause disease in future generations. Remarkably, it appears that early life exposures can lead to health problems not only in adulthood, but also down through subsequent generations. For instance, adult diseases linked to newborns’ low birth weight, enumerated above, cause adverse effects not only in those babies born small, but also in their children of any birth size, through heritable changes in gene expression that result in a phenomenon known as “epigenetic inheritance.” Very different from genetic mutations, which are physical changes in gene structure, epigenetic inheritance is instead characterized by certain genes being turned on or off, but near permanently in ways that can be inherited.
If a genetic mutation is like changing a light fixture, the comparable epigenitic change would involve taping the light switch on or off. Since genes are responsible for making the chemicals that build and repair the body, this unnatural forcing to a permanent on or off position can have far-reaching consequences. In humans, both kinds of genetic changes, mutations as well as epigenetic changes in gene expression, can be passed down to a baby in the womb.
Scientists have recently found heritable epigenetic changes linked to the fungicide vinclozolin and pesticide methoxychlor, which impaired sperm counts and sperm motility not only among animals exposed in utero, but also in three subsequent generations (Anway et al. 2005). In other words, what each of us was exposed to in our mother’s womb might affect the health of our great-grandchildren.
Notably, both of these pesticides were recently banned under a federal law that requires pesticides to be safe for newborns and children. The government gives children no explicit protection under the federal law meant to ensure the safety of other commercial chemicals (the Toxic Substances Control Act), even though risks from childhood exposures to industrial chemicals are no lower than those from pesticides.
Cord blood pollutants in this study, linked to health problems. Scientific studies implicate some of the chemicals we detected in cord blood with serious, ongoing human health problems:
Dioxin exposures during fetal development have been implicated in endocrine-related cancers in women (breast and uterine, for example) by altering hormone levels, increasing the sensitivity of children and adolescents to other carcinogens (Birnbaum and Fenton 2003). In men, tiny levels of dioxin in the range of 0.02 to 10 parts per billion alter testosterone levels and are linked with diabetes (EPA 2004a). Dioxin at 80 parts per trillion in paternal — but not maternal — serum causes a significant change in the sex ratio of children (Mocarelli, et al. 1996, Mocarelli, et al. 2000). At this tiny dose, men father nearly twice as many girls as boys. As body burdens increase within and above these ranges, the likelihood, severity, and potential spectrum of non-cancer effects increases (EPA 2004a). Fetal dioxin exposure can harm the immune system, thyroid, and brain (Van Loveren et al. 2003, Faroon et al. 2001, ten Tusscher and Koppe 2004). Dioxin from garbage incinerators is associated with increased incidence of infant death and birth defects (Tango et al. 2004).
Methylmercury exposure in the womb causes measurable declines in brain function in children exposed to levels corresponding to 58 parts per billion in maternal blood (NAS 2000b). Researchers in the Netherlands found a doubling in the risk of heart attacks and death from coronary heart disease at methylmercury hair levels of 2 mg/kg, which corresponds to about one fifth the assumed safe maternal blood level (Salonen, et al. 1995). Increased diastolic and systolic blood pressure and decreased heart rate variability in developmentally exposed children have also been observed at doses below what the EPA considers a safe maternal blood level (NAS 2000b, Sorensen et al. 1999).
PCBs at 9.7 ppb in maternal serum during fetal development can impair brain development, with resultant attention and IQ deficits that appear to be permanent (Jacobson and Jacobson 1996). Notably, IQ deficits are linked to the mother’s PCB levels, not the PCB levels in children at 4 and 11 years of age (by which time the children’s PCB levels had decreased substantially compared to levels at birth), underscoring the limitations of studies that look for correlations between current body burdens and health effects in the absence of data on in utero exposures. Levels of PCBs in the general population are also associated with abnormal menstrual cycles (Cooper et al. 2005).
DDE above 15 ppb in maternal blood is associated with preterm birth and low birth weight, with weight corrected for gestational age (Longnecker et al. 2001). DDE is a metabolite of the banned, persistent pesticide DDT. Using the associations derived from tests of archived blood samples from a pool of 42,000 women, researchers estimated that DDT exposures in the U.S. population could have accounted for up to 15 percent of infant deaths during the 1960s. Low birth weight is recognized as a risk factor for type II diabetes, high blood pressure, and cardiovascular disease later in life (Prentice and Moore 2005, Godfrey and Barker 2001, Hales and Barker 2001). Even if these lower birth weight babies “catch up” later, the damage may have already been done. A substantial number of studies have found that low birth weight followed by an accelerated growth rate during childhood is a significant risk factor for high blood pressure, stroke, insulin resistance and glucose intolerance (Eriksson, et al. 2000a, Eriksson, et al. 2002, Eriksson et al. 2000b, Eriksson et al. 1999, Eriksson and Forsen 2002, Forsen et al. 2000, Ong and Dunger 2002, Stettler et al. 2002).
Some facts about human health trends
Cancer. Cancer incidence has steadily increased over the decades for many forms of the disease, including breast, prostate, and testicular (NCI 2005). The incidence of childhood cancer increased by 27.1 percent between 1975 and 2002, with the sharpest rise estimated for brain and other nervous system cancers (56.5 percent increase) and acute lymphocytic leukemia (68.7 percent increase). The incidence of testicular cancer also steadily rose 66 percent between 1975 and 2002 (NCI 2005). The probability that a U.S. resident will develop cancer at some point in his or her lifetime is 1 in 2 for men and 1 in 3 for women (ACS 2004). A broad array of environmental factors plays a pivotal role in the initiation and promotion of cancer. Just 5 to 10 percent of all cancers are directly linked to inherited, genetic factors (ACS 2001).
Breast cancer. Among girls born today, one in seven is expected to get breast cancer and one in 30 is expected to die from it. Invasive female breast cancer increased an average of 1.5 percent per year between 1973 and 1996, for a total increase of 25.3 percent. Among those 65 and younger, breast cancer incidence rose 1.2 percent per year, corresponding to a doubling every two generations (58 years). If trends continue, the granddaughters of today’s young women could face a one in four chance of developing breast cancer (NCI 1996, NCI 1997).
Testicular cancer. At its current pace, the incidence of testicular cancer is doubling about every one and a half generations (39 years). In the U.S. the incidence of testicular cancer rose 41.5 percent between 1973 and 1996, an average of 1.8 percent per year (NCI 1996, NCI 1997). Testicular cancer is now the most common cancer in men age 15 to 35 (NCI 2005).
Prostate cancer. Prostate cancer rates rose 4.4 percent a year between 1973 and 1992, or more than a doubling of risk in a generation. Since 1992, the incidence has declined, but it is still 2.5 times its 1973 rate. Part of this increase can be explained by better detection, but increased incidence has also been accompanied by an increase in mortality – which better detection cannot explain. Prostate cancer is now the most common cancer among U.S. men, and the second most lethal, killing an estimated 31,900 men in the year 2000 alone (NCI 1996, NCI 1997).
Major nervous system disorders. Several recent studies have determined that the reported incidence of autism is increasing, and is now almost 10 times higher than in the mid-1980’s (Byrd 2002, Chakrabarti and Fombonne 2001). The number of children being diagnosed and treated for attention deficit disorder (ADD) and attention deficit hyperactivity disorder (ADHD) has also increased dramatically in the past decade (Robison et al. 1999, Robison et al. 2002, Zito et al. 2000). The causes are largely unexplained, but environmental factors, including chemical exposures, are considered a likely contributor. Environmental factors have also been increasingly linked with Parkinson’s disease (Checkoway and Nelson 1999, Engel et al. 2001).
Preterm births and low birth weights. Preterm births have increased 23 percent over the past 2 decades; low-weight births have become more common (Ananth et al 2001, Branum and Schoendorf 2002). The causes are largely unknown, but environmental factors such as chemical pollutants and nutrition are thought to play a role. Low birth weight has been linked to adult obesity, diabetes, cardiovascular disease, schizophrenia, and other conditions (Barker 1995, Wahlbeck et al. 2001, Thompson et al. 2001, Hales and Ozanne 2003). It has also been linked to lower academic performance, neurosensory impairment, and lower rates of pregnancy in the offspring (Hack et al. 2002).
Defects of the reproductive system. Studies show that sperm counts in certain parts of the world are decreasing (Swan, et al. 2000, Toppari, et al. 1996). Scientists have measured significant regional differences in sperm count that cannot be explained by differences in genetic factors (Swan et al. 2003). Girls may be reaching puberty earlier, based on comparing current appearance of breast development and pubic hair growth with historical data (Herman-Giddens, et al. 1997). Rates of hypospadias, a physical deformity of the penis, have risen in recent years (Paulozzi et al. 1997). The incidence of undescended testicles (cryptorchidism) and testicular cancer also appear to be rising in certain parts of the world (Bergstrom et al. 1996, McKiernan et al. 1999, Toppari et al. 1996, Paulozzi 1999). Several studies have suggested links between developmental exposure to environmental contaminants and cryptorchidism or testicular cancer (Hardell, et al. 2003, Hosie, et al. 2000, Toppari, et al. 1996, Weidner, et al. 1998).
Declining sperm count. An analysis of 101 studies (1934-1996) by Dr. Shanna Swan of the University of Missouri confirms results of previous studies: average sperm counts in industrialized countries appear to be declining at a rate of about one percent each year (Swan et al. 2000).
Hypospadias. Incidence of hypospadias, a birth defect of the penis, doubled in the United States between 1970 and 1993, and is estimated to affect one of every 125 male babies born (Paulozzi et al. 1997). Data from the Centers for Disease Control and Prevention show that rates in the U.S. began climbing in about 1970, and continued this increase through the 1980s. This condition is a physical deformity of the penis in which the opening of the urethra occurs on the bottom of the penis instead of the tip.
Undescended testicles. This birth defect, where testicles fail to completely descend into the scrotum during pregnancy, occurs in two to five percent of full-term boys in Western countries. Rates of the defect increased greatly in the U.S. in the 1970s and 1980s. Men born with this defect are at higher risk for testicular cancer and breast cancer (Paulozzi 1999).
Together with 287 industrial pollutants in 10 newborn babies, this body of science and the litany of serious, continuing human health concerns reveals the critical need for reform of our system of public health protections, which fails to require proof that chemicals are safe for children.