"Pesticides May Affect Penis Size, " runs the headline in the London Free Press. The first paragraph alarmingly reports that "A renowned U.S. scientist who has documented fertility and sex changes—including decreasing penis size—due to environmental contamination says he wouldn't apply pesticides on his own lawn."
Whose sexual organs was the renowned scientist talking about? Alligator penises. Specifically, the penises of some American alligators that grew up in Florida's most polluted lake. In 1980 a massive industrial pesticide spill drained into Lake Apopka, contaminating it with high levels of pesticides with anti-androgenic activity. The toxins clearly had deleterious effects on wildlife. The renowned scientist cited in the article is University of Florida researcher Louis Guillette, who also apparently asserted, "This is important because it is not just an alligator story. It is not just a lake story. We know there has been a dramatic increase in penile and genital abnormalities in baby boys."
One sometimes gets the impression from some scientists and activists that pesticides are just pure evil developed by wicked corporations for the purpose of poisoning people, not substances devised to protect crops or eradicate disease-carrying vermin. In any case, since it turns out that activists were wrong when they claimed that pesticides were causing a cancer epidemic, then surely the chemicals must be doing something else vile. How about hitting men where it really hurts? That'll get their attention!
But is it true there has been a "dramatic increase" in penile abnormalities? The evidence is equivocal. A major scientific review in 2005 found that male congenital anomalies had increased from 7 per 1000 in 1988 to 8.3 per 1000 in 2000. Interestingly, the same study found that the higher a family's socio-economic status, the higher the risk that a boy would be born with penile abnormalities. Another study found higher than expected rates of male genital deformities among newborns in some parts of the Netherlands. Specifically, researchers found a correlation between a father's exposure to pesticides and the probability of cryptorchidism (failure of one or both of the testicles to descend into the scrotum) in his newborn son. There was no correlation between paternal and maternal pesticide exposure and the incidence of hypospadias (a genital defect in which the urethra opens on the underside of the penis rather than at the end).
On the other hand, there is a plethora of studies that find no recent increase in penile defects. For example, in 2003 a California study lasting 13 years and funded by the March of Dimes found "there was no evidence for an increase in prevalence "of hypospadias. And a 2004 Scottish study in the British Medical Journal reported that "A new linked register of congenital genital anomalies in Scotland suggests that over a decade, the birth prevalence of genital anomalies has changed little. " Ditto for Finland and New York State. And a 2005 study in Washington State study found "the prevalence of hypospadias in Washington State did not increase significantly between 1987 and 2002."
Even a 2005 study specifically trying to correlate exposure to organochlorines with male genital abnormalities found none. In that study, researchers compared the levels of pesticide residues in the blood serum of women whose boys were born with malformations with women whose boys were not did. They reported, "Our study does not provide epidemiologic support for a causal adverse relationship between DDT or DDE and cryptorchidism or hypospadias."
But there is another puzzle—exposures to many of the most suspect pesticides have been declining for decades. A 2002 study of synthetic chemical residues in human breast milk supported by an activist group, the Natural Resources Defense Council, concluded, "Over the past few decades, levels of the organochlorine pesticides, PCBs, and dioxins have declined in breast milk in countries where these chemicals have been banned or otherwise regulated." A report from the American Council on Science and Health in New York which receives some industry support asserts that the residues of many organochlorine pesticides found in human tissues declined by 90 percent. So if exposure to pesticides is declining, why would male genital abnormalities be going up?
The Washington State study points to one possibility. It found one factor that correlated with an increased incidence of hypospadias?maternal age. In 2001, another study by Columbia University urologist Harry Fisch also found that the incidence of hypospadias increased with maternal age. As Fisch notes the number of live births to women over age 35 has increased from 6 percent in 1980 to over 12 percent today. The comprehensive 2005 study that found an increase in hypospadias noted that it also correlated with higher socio-economic status which tends to be linked with higher maternal age.
As far as I know, no one has done a study comparing the penis sizes of newborn boys and pesticide exposure. However, researchers at the University of Rochester in New York reported in 2005 that the distances between the anal openings and the scrotums (anogenital distance or AGD) of boys whose mothers had relatively higher levels of plasticizers known as phthalates in their urine were less than those whose mothers had lower levels of phthalates. This effect had been previously observed in rodent pups that had been exposed to phthalates prenatally in the lab. But keep in mind that none of the 134 boys in the Rochester study had malformed genitals.
Not surprisingly, some in the industry disagreed, arguing, "Because little is known about AGD in human infants and its variation, no conclusion can be drawn whether the reported values are normal or abnormal. The range of AGD values seen among study subjects likely represents typical biologic variation that would be expected to occur among normal study subjects." Curiously, the Rochester researchers responded, "First, because all infants in our study appeared normal, [industry scientists] infer that there is no evidence of an adverse effect. However, the absence of evidence of an effect in infancy does not preclude serious adverse effects in later life. "
One could also say that the absence of evidence for an armada of gigantic purple space squid massing behind the moon for an invasion of the earth doesn't mean that they won't show up later—but never mind. Perhaps the Rochester study will be replicated and eventually show that phthalates are responsible for actual deleterious effects on the health and fertility of people, or perhaps its findings will dissipate in the light of further research just as those that initially supported the notion of a synthetic chemical cancer epidemic did.
Make no mistake about it—massive occupational exposure in the 1970s and 1980s to some pesticides had tragic health effects such as causing infertility in hundreds of agricultural workers. But so far, the effect of low level exposures to pesticides and other synthetic chemicals on human male genitalia does not appear to have been "dramatic" and may not exist at all. Dueling ambiguous scientific studies bring to the fore a hard policy question: How much time and resources do we (government, industry and consumer) want to spend in chasing what have so often turned out to be phantom risks? In the meantime, spraying a lawn for dandelions and fire ants doesn't seem like taking much of a risk with one's manhood to me.