“A theory that explains
everything, explains nothing.”
― Karl Popper1
A
column by Nick Kristof in the New York Times first alerted me to a newly
published book entitled Count Down: How Our Modern World Is
Threatening Sperm Counts, Altering Male and Female Reproductive Development,
and Imperiling the Future of the Human Race, co-authored by Shanna Swan, an epidemiologist, and Stacey
Colino, a journalist. True to its title,
the book tries to make the shocking case that environmental exposures to trace
levels of certain chemicals, particularly a diverse group called phthalates,
are responsible for causing severe declines in various measures of male and female
reproductive health and are placing the entire human race at threat of
extinction. These chemicals are purported to act by disrupting the endocrine
systems of humans and other species and hence are referred to as EDCs. However, this sensational claim is neither
new – Swan has dedicated at least the past 25 years of her career to making it,
and Kristof has devoted at least several of his opinion columns2
over the past decade shamelessly promoting it – nor is the scientific evidence
they offer to support it very convincing.
As Carl
Sagan once stated, "extraordinary claims require extraordinary
evidence”, and by this test Swan and her book get failing grades.
I’m not alone in my criticisms, as other scientists have
also panned the evidence. Responding to
Kristof’s column, Geoffrey
Kabat, an academic epidemiologist and author of the book “Getting Risk Right: Understanding the
Science of Elusive Health Risks”, which includes an entire chapter
devoted to the EDC hypothesis, wrote: “Kristof’s commentary, and in fact the
research that he selectively cites, tell only part
of a complex story about the impact of exposure
to environmental chemicals. Rather than
conveying the grays of science, he ends up promoting
the most sensational, almost black and white, and least probable
explanations of a serious environmental and health issue.”
Kabat
has offered similar criticisms of a prior Kristof column on the topic, as
has Dr.
Paul Turek, an internationally renowned expert in men’s sexual health and
reproductive urology, who has pointed out that the reported decline in sperm
counts derives from flawed epidemiology studies, and that the reported level
of decline still leaves the vast majority of men well within what is widely
considered to be the normal and healthy range.
After reading Swan’s book, Tom Chivers, a
book author himself and science editor, wrote “But the book does not seem
sensible. Because for Swan, everything
causes fertility problems, not just phthalates. Sugar, beef, cycling,
stress, watching TV, doing too much exercise, doing too little, eating the
wrong diet; you can barely get out of bed in the morning without sabotaging
your chance of having a baby. Undergoing stress and trauma will not only make
you less fertile, they’ll affect your children’s fertility (should you remain
capable of having them). And phthalates and other EDCs don’t just damage your
chance of having a baby – they seem to be the cause of everything wrong in the
world.”
Reading Chivers review I was reminded of the quote from the noted
science philosopher, Karl Popper, “A theory that explains everything,
explains nothing.”
Furthermore, at no point in the book do Swan and Colino even
try to explain in any detail their theory of how EDCs supposedly interact with
other risk factors to cause the harm they allege. It is simply presented as established
science, which is far from the truth. But the problems with the book run much broader
and deeper, as I explain in greater detail below.
Strengths of the Book
Count Down
is not wholly without its merits. Swan
and Colino deserve some credit for bringing attention to infertility, a topic
of great interest to prospective parents who are struggling to conceive. My wife and I started our family while we
were quite young and were blessed to have children when we wanted them. We took our fertility for granted. By contrast, our children and their spouses chose
to start their families in their 30’s, and while they were also ultimately
successful, on average it took them quite a bit longer to conceive. This created lots stress for them and for us,
as we were anxious to have grandchildren while we still had our health to enjoy
them. Unfortunately, some other couples,
including friends of ours, have not been as lucky. So this is a serious issue for some
individuals. For broader society? Perhaps not so much!
Swan and Colino devote several chapters to explaining the
underlying biology of male and female reproductive development, and do a decent
job of it, although I’m almost certain that more than a few clinicians will
object to some of their more fanciful characterizations and claims,
particularly as they pertain to small changes in sperm count and morphology. The book also includes a chapter that is focused
on the long list of non-chemical risk factors for adverse reproductive health,
including: age,
heat, obesity, smoking, radiation, marijuana use, vaping, alcohol use, a wide
variety of medications (including opioid use), diet, exercise, psychological
stress, other medical conditions, and other exposures. Their list, while not as exhaustive as others
I have seen published, is reasonably complete and captures the most
well-established and impactful of the known factors.
Major
Problems with the Book
In
addition to the problems that were noted at the outset of this article, namely:
n
The claims are overly dramatic, which Chivers
attributes to Swan not believing that her issue is getting enough public
attention, so to compensate she has overhyped it by writing a “polemic” and has
done so in the style of “the
fallacy of reversed moderation” which “…ends up looking obsessive and
weird” (Indeed, lending credence to this notion, late in the book the authors
confess to wondering why the issue hasn’t generated more public outrage); and
n
the theory that EDCs cause everything simply
lacks biological plausibility;
the book suffers from numerous other problems that mislead readers
who are not familiar with the underlying science.
The Authors Views Are Extremist and NOT in the Mainstream
The authors fail to provide any perspectives on the issue other than
their own. The endocrine hypothesis was introduced more than 30 years ago
and has been steeped in controversy ever since. For a fascinating tour de force outlining this controversy
I highly recommend the reader look at a doctoral
dissertation by Alexis Abboud.
Abboud carefully chronicles the evolution of the hypothesis and
discusses how its proponents quickly abandoned doing good science in favor of
active lobbying for policy changes. None
of that controversy is discussed in Swan’s book, which consequently leaves the
reader to mistakenly believe that the scientific community has reached
consensus on it and that Swan’s opinions are in the mainstream. Nothing could
be further from the truth. At least
Kristof included a paragraph devoted to the uncertainties and speculative
nature of the EDC hypothesis, although he buried it late in his op-ed, only
after making his most outrageous claims.
Remarkably, Swan does nothing of the sort.
As Kabat
writes “Missing from Kristof’s column [and notably also from
Swan’s book] is any understanding that the scientists he quotes
are not representative of views in the scientific
community. A very different picture emerges when one listens
to some of the foremost authorities in the field of reproductive
health.” Kabat
goes on to quote from Sir Richard Sharpe one of the world’s foremost
endocrinologists. He is the research scientist who originated the notion and
study of ‘endocrine disrupting chemicals’ in the 1990s. After participating in and reviewing hundreds
of studies on EDCs, Sharpe is convinced the concept is wrongheaded—an
ideological belief and not science based. Kabat
makes a further important point “Unfortunately, by leveraging the media
(and often partnering with tort lawyers), these ‘advocacy
scientists’ generate massive reams of dubious-quality
research, sucking up the bulk of public funding that should
be devoted to the more difficult work of elucidating the complex pathways of
healthy reproductive development.”
Near Exclusive Focus on Sperm and Egg Count and Quality
and Fertility is Misplaced
Turek
largely dismissed the importance of sperm and egg counts and quality and even
fertility3 (the number of live births per unit of population) as
measures of reproductive health and has instead emphasized the importance of
measuring fecundity – the potential to conceive. Turek
recounted the findings of a NIH
sponsored scientific meeting in which he was a participant that examined
the question of decreased fecundity and concluded there is no hard evidence to suggest that this has changed at all.
Turek
further explained “… what surfaced early on and pervaded the entire meeting
were the massive complexities that surround this subject. Factors such as
cultural norms, socioeconomics, family planning behavior and pregnancy
intentions are all rather large elephants in the room when discussing human
fecundity. And they are all huge influencers about which very little is known.”
No Context is Provided for Evaluating Epidemiological
Evidence
Much of the research that Swan cites to support her claims
derives from observational epidemiology studies rather than from controlled
experiments. Yet, she never discusses
the inherent limitations of such studies – notably how they are fundamentally
less rigorous than experimental studies and thus are far more prone to yielding
unreliable findings due to chance, confounding and bias4. As a rule,
epidemiologists do not put much stock in the findings from single, small,
un-replicated studies. They are too unreliable. Much of the work Swan cites on EDCs derives
from such studies and particularly from cross-sectional studies which are
considered among the weakest study designs.
I have written previously on this blog about these topics and I refer
the reader to those articles for the details (see Bond
2019, Bond
2017, Bond
2016).
Epidemiologists want to see consistent results generated
across multiple studies of different designs, conducted by different
investigators acting independently, before they are convinced that the findings
are likely to be real rather than due to artifacts. In fact, Stanford epidemiology professor John
Ioannidis wrote a seminal paper proving that most published research
results are false. The consequence of
Swan’s failure to provide this essential context is to leave the reader with
the mistaken impression that the science supporting her claims is more robust
than is actually the case.
Although earlier I gave credit to Swan and Colino for
including a chapter devoted to non-chemical risk factors, there are several glaring
problems with the evidence they presented which need to be highlighted. Firstly, much of that evidence also derives from
observational epidemiology studies. However, Swan fails to make any attempt to
characterize that evidence in terms of the number of studies, their design or
size, consistency of findings, measures of the strength of association, etc.
that would allow the reader to understand how compelling that evidence is,
especially when compared and contrasted with the evidence she cites to support
a link with EDCs. Which of the many
non-chemical risk factors are most likely to negatively impact reproductive
health and what is their relative contribution compared to one another and to
EDCs?
Unlike the evidence she cites on industrial chemicals which
comes from a few poorly designed studies based on small numbers and that yield
weak associations, much of the evidence on these other factors derives is much
more robust (i.e., more numerous, better designed and larger studies with
stronger associations reported). Moreover, she does not discuss how
these other factors may actually interfere with or confuse the studies done on
environmental chemicals (a phenomenon which epidemiologists refer to as
confounding) if the investigators do not measure them and control for their
influence in their studies. Again, the uninformed reader will be misled.
By her silence on these important topics, most readers of
the book will mistakenly assume that the evidence is equally scientifically
robust and that all of the various risk factors are equally potent in
increasing the risk of reproductive harm.
Neither is true.
The Authors “Cherry Pick” the Science, Do Not Weigh the
Evidence and Mistakenly Assume Correlation Equals Causation
The chapter which presents the evidence that Swan alleges
shows exposures to purported EDCs are an important contributor to adverse
reproductive health effects is surprisingly short – only 18 pages in length or about 8% of the
total pages in the book (not counting the bibliography or index) -- and it is
shockingly superficial. Separate
sections are devoted to phthalates, Bisphenol A (BPA), polybrominated flame
retardants (PBDE’s), pesticides and what Swan refers to as “under the radar
EDCs” which she lists as perfluoroalkyl substances (PFAS), Polychlorinated
Biphenyls and dioxin.
Early in the book, Swan describes phthalates as a large and
diverse set of chemicals, but later she lumps them all together and claims they
need to be considered as a single class without providing any scientific
justification for doing so. She does the
same for PFAS, PBDEs and most crazily for pesticides, a very diverse set of chemistry. The
American Chemistry Council’s High Phthalates Panel, which represents US producers
of these chemicals, has strenuously objected to treating the diverse chemicals
as a single class, noting their widely divergent toxicology profiles. Other ACC
chemical panels have expressed similar objections (PFAS, and Flame
Retardants).
Swan does not reveal which literature sources she searched
to identify pertinent studies or the criteria she used to include some and
exclude others from consideration. Nor does she discuss how she evaluated the
quality of the individual studies or reconciled or weighted their disparate
results. Further she does not
share her criteria for assessing the likelihood that mere statistical
associations are likely to represent causal ones. This is a major departure from standard
scientific practice which demands a high degree of transparency on these
critical steps.
Swan often contradicts herself on the weight of the evidence5
linking EDCs to adverse health effects.
Sometimes she refers to “associations” and other times she strongly
states her personal belief that the relationships are causal. Yet, most scientists who have examined the
same evidence have concluded that it falls far short of standards for
establishing causation. So, Swan and
Colino quite often are guilty of mistakenly assuming mere statistical
correlation equates to causation.
This is a common fallacy that the media unwittingly promotes; however,
readers should expect better from an academic scientist.
Kabat
noted many of the same points I observed when evaluating the evidence Swan
relied upon. She cites isolated results from poor quality studies, which
haven’t been reproducible, and selectively ignores the most well conducted
studies and scientific discussion that provide no support for the claim that
reproductive health is under threat.
Epidemiology studies claiming declines in sperm quantity and quality
rarely take into account some of the most important risk factors, such time
since last ejaculation, scrotal temperature, prolonged sitting, season,
smoking, drug use, stress, trauma, obesity, under-nutrition, medications, and diets
and as a consequence they are prone to confounding and yielding misleading
results. Swan also claims that
malformations of the male genitals are on the rise. This is not supported by systematic reviews
of the scientific evidence. Furthermore,
she highlights the rising incidence of testicular cancer and strongly infers a
role for EDCs in causing it, but there is strong evidence to support that rise
actually started in the early twentieth century and had its roots in early life
exposures in the late nineteenth or early twentieth century, which casts strong
doubt on the hypothesis that the increase can be explained by exposure to
chemicals in the post-World War II environment.
Finally, Swan includes a brief discussion of three examples
she offers of “regrettable substitutions” for one type of phthalate (DEHP),
PBDEs and BPA wherein the substitute chemicals, according to her, turned out to
be equally bad or worse. However, she provides no real substantive
evidence to support her claims. I’m
personally astonished at how the proponents for the endocrine hypothesis are so
quick to claim “regrettable substitution” on the flimsiest of evidence and take
no accountability for their role in causing it.
They produce substandard science indicting chemicals and then work hand
in hand with activists to exert tremendous public and marketplace pressure on
users of those chemicals to quickly deselect them from their products. Its no
wonder that in their haste to escape the harsh spotlight that the users will
jump to the next available chemical that provides the functionality they
desperately need at a competitive price.
Swan is quick to praise the large retail chains for their efforts to pressure
their suppliers to deselect chemicals, but she fails to acknowledge that those
same retail chains demand that the formulators not pass along any increase in
the cost of the consumer products they peddle.
It should be no surprise then, that some of the users might consequently
cut some corners in choosing replacement chemicals.
Potency and Dose are Completely Ignored
It is a fundamental tenet of toxicology that the dose makes
the poison. This is credited to
Paracelsus who wrote "All things are poison, and nothing is without
poison; the dosage alone makes it so a thing is not a poison." Yet,
Swan never discusses the dose levels she suspects are required to cause the health
effects she alleges. In reality, evidence from animal toxicology studies,
including reproductive and developmental studies, are available for many of the
purported EDCs, especially pesticides, and safe levels of exposure have been
established to protect against the adverse effects Swan alleges. Endocrine
pharmacology and medical toxicology establish that safe levels of exposure
exist for endocrine active chemicals, both natural and man-made. Biomonitoring data on
samples of the general population generally confirms that exposures are usually
well below levels of concern. The
US EPA perhaps states it best, “…limited evidence exists for the potential of
chemicals to cause these effects in humans at environmental exposure levels.”
It’s not only the dose, but also the potency of a substance,
that determines its effects. Once again, Swan does not discuss the relative
potency of the chemicals she indicts.
The reality is that synthetic
EDCs are much less potent in interacting
with the endocrine system than many naturally occurring endogenous and
exogenous EDCs.
To illustrate that her hypothesis that EDCs are capable of
causing multigenerational health effects, Swan cites the well documented example
of Diethylstibestrol (DES), a drug once
prescribed during pregnancy to prevent miscarriages or premature deliveries.
It was later found to cause a rare form of vaginal cancer in the young adult
daughters born to women who took the drug. Yet extrapolating from the DES example to
industrial chemicals in the ambient environment is very precarious indeed, and
unreasonable on several levels. DES is a
very potent endocrine active agent – orders of magnitude more potent than the
industrial chemicals Swan is indicting, and it was taken orally in therapeutic
doses which greatly exceed the trace levels of exposure to those same
industrial chemicals (Golden
et al, 1998; and Borgert
et al, 2012). Thus, the DES
story, however tragic, cannot be reasonably extrapolated to the trace
environmental levels of industrial chemicals. Swan also promotes some of the more
controversial aspects of the “fashionable”
field of epigenetics and posits that environmental exposures, lifestyle
choices we make, and even emotions we feel can be passed on to future
generations. It
is presented as if there is scientific consensus about it, which is highly
misleading.
Toward the
end of the book Swan briefly mentions the controversial non-monotonic,
low-dose hypothesis, but as
she does with most of the science in her book, she treats it very
superficially. Contrary to the
well-established toxicology principle that “the dose makes the poison,” some
scientists and advocacy groups allege that in certain circumstances, a
different dose-response interaction can possibly occur with alleged EDCs. The
researchers speculate that a more significant response could occur at a low
dose, compared to that observed at higher doses. These “low-dose effects” are
postulated to occur at doses well below those levels previously tested and
determined to be safe by regulatory authorities. Although this non-monotonic, low-dose
hypothesis is often discussed in relation to endocrine-related science,
scientists at regulatory agencies across the globe, including the EPA and
European Food Safety Authority (EFSA), have argued that the hypothesis could,
in theory, apply to all chemicals, regardless of the mechanism by which they
cause toxicity.
Some of those
same regulatory
agencies also have conducted rigorous reviews and have been unable to validate the non-monotonic, low-dose
hypothesis using reproducible, relevant testing.
Furthermore,
EPA led a work group of scientific experts that reviewed various studies, and
the conclusion of the group’s draft
report affirms what
mainstream scientists have said for years: the purported scientific evidence
for the nonmonotonic, low-dose hypothesis, even as it might apply to endocrine
active chemicals, is, at best, very weak.
Evidence Supporting Similar Effects in Other Species
Swan also claims that EDCs are causing similar threats to
the reproductive health of other environmental species, but once again she is
guilty of selectively telling only the parts of the story that support her
hypothesis and ignoring anything that contradicts it. Among the examples she cites is the work
conducted by Louis Gillette on alligators which he sampled
from a part of Lake Apopka, Florida that had been heavily contaminated with
pesticides, many of which were eliminated from use decades ago. Hardly representative of the trace level
exposures that are more likely to be endemic to their broader habitat. The
current reality is that the alligator and crocodile populations in the
southeastern U.S. have robustly rebounded. This has been the result of
protections established since the late 1960’s to guard against the most
well-established threats to their health, NOT chemicals as Swan implies, but
rather due to excessive market harvesting, poaching and loss of wetland
habitat.
Chivers rightfully
takes Swan to task for yet another example she cites, the recently noted
declines in insect and bird populations.
Although the
scientific community has speculated on a variety of potential causes for this
phenomenon, Swan ignores any non-chemical related explanations such as climate
change, loss of habitat, etc. and focuses solely on EDCs, but then presents
scant scientific evidence to support it. Once again, this omission will
mislead the uninformed reader to assume that the broader scientific community
believes EDCs are the primary threat.
Swan’s
Recommended Actions for Remedying the Problem Are Uniformly Ill-Considered
The final three chapters of the book are dedicated to Swan’s
recommendations of steps that can be taken to (1) improve reproductive health
through better personal lifestyle choices, (2) efforts to reduce personal exposures
to purported EDCs, and (3) changes to public policy, respectively.
To their credit, the authors first recommend good lifestyle
choices, presumably because these are the most well-established risk factors
and are most impactful, but they never really come out and say so directly
which is unfortunate. Avoid tobacco use, maintain a healthy weight, eat
smartly, exercise, and avoid unhealthy stress. Of course, such actions
will help prevent a myriad of other adverse health events as well. The authors miss an opportunity to prioritize
even these factors according to which ones will deliver the biggest bang for
the buck, which would have been helpful to readers especially since making even
one major change in lifestyle choices at a time can be an exceptional personal
burden for most individuals.
Next up they offer a room-by-room approach to reducing
chemical exposures in your home, mostly focused on phthalates, BPA, PBDEs and
pesticides. Much of this advice is neither practical to implement nor
scientifically justified, and once again it is just thrown over the fence with
very little prioritization as to what might be the most cost-effective steps for
people to take. Those who are
socioeconomically disadvantaged, and who are also most likely to have other
risk factors for poor reproductive health, will find it nearly impossible to,
for example, buy organic produce; buy and eat animals labeled with USDA organic
seal; filter their drinking water; replace their couches and wall to wall
carpeting, and so on. As such, the
advice comes across as directed at a small subset of the population that can
afford to obsess about such issues. She
directs readers to the Environmental Working Group (EWG) website for lists of
“safer” cleaning and personal products.
As Kabat points out some of the advice such as getting rid
of your vinyl shower curtain, is just downright ridiculous because any
off-gassing of EDCs from it has got to be infinitesimally small and of no
health consequence. Kabat also takes
pains to point out the lack of scientific rigor in EWG’s “safer” products
assessments, writing “It’s also troubling that Kristof and Swan tout the
Environmental Working Group, an environmental advocacy group funded in
part by the organic industry [read the GLP Profile of the Environmental Working Group]. EWG is notorious for not
following standard protocols for measurement of pesticide residues in
produce. It is also notorious for putting out an annual “Dirty
Dozen” list of ‘pesticide soaked’ fruits and vegetables that is widely
decried as scientifically illiterate (here, here, here), including by the USDA, during the Obama Administration.”
The public policy changes Swan calls for are
ill-conceived and are based on her misinformed and distorted views of current
chemical industry practice and regulatory differences between the U.S. and
Europe. She and Kristof both
misrepresent the chemical industry’s efforts to respond to the endocrine
hypothesis. I was there at the beginning
in the early 1990’s and have continued to be engaged ever since, and can
personally attest to the
seriousness with which the industry has always taken the issue. Anything less would be a dereliction of
fiduciary responsibilities. Working as individual companies and through ACC, and the
International
Council of Chemical Associations (ICCA), the industry has and continues to
constructively contribute by helping to scientifically develop and validate proposed
endocrine screens and tests, conducting those screens and tests on priority
chemicals, and funding novel science and organizing scientific meetings through
their Long-Range Research Initiatives. Individual companies are incorporating
environmental, health, safety and sustainability concerns, including endocrine
into the earliest stages of new product development, and are employing the
latest predictive toxicology and exposure tools to do so. In today’s environment, it simply doesn’t pay
to “rathole” money invested on prospective products that will fail to meet
marketplace or regulatory hurdles.
Swan, and then by
extension Kristof, also claim that while Europe and Canada are regulating EDCs,
the US is not. Again, this is simply not
true, and their description of what is actually happening is incomplete and
distorted. For instance, she
ignores the fact that the EPA
has established a science-based endocrine disruption screening and testing
program (EDSP) for determining
which substances have the potential to interact with the endocrine system.
Substances with such potential may then be further evaluated by EPA to
determine whether adverse effects can occur and what exposures might trigger
such responses. Chemicals that are found to cause adverse effects are subjected
by EPA to a comprehensive risk assessment, so researchers can understand the
potential for exposure to the chemical and the likelihood of harm under
real-life scenarios. This
science-based risk assessment helps scientists determine the difference between
the levels of exposure that can produce adverse effects, and the typical
exposure levels experienced by humans and wildlife. EPA then determines if this safety standard is appropriate to protect
public health and the environment, including groups that might be particularly
sensitive, or if limiting certain uses of the chemical should be considered. Swan also completely ignores the considerable
international efforts through OECD to advance approaches to endocrine screening
and testing.
Finally, Swan also
makes the case for implementing the Precautionary Principle (PP) to ban EDCs,
and argues that the EU does this whereas the US does not. Such claims have been thoroughly investigated
and found to be incorrect. A full discussion of the problems with the PP
is beyond the scope of this review, but I refer the reader to the writings of Jonathon Adler and Cass Sunstein, who served in the Obama administration,
both of whom argue the PP is flawed, incoherent and unnecessary since
precaution is already adequately incorporated into existing US health and
environmental laws and regulations.
In Conclusion
n
The book brings attention to infertility, a complex
topic of great interest to prospective parents who are struggling to conceive.
n
However, the authors dramatically overstate
their case and fail to provide convincing scientific evidence to support their
hypothesis that trace levels of synthetic chemicals (purported EDCs) in the
environment are playing a meaningful role in causing infertility and
threatening the human race with extinction.
n
They undercut the biological credibility of
their hypothesis by asserting that trace levels of EDCs cause a wide range of
adverse health effects. They
oversimplify a very complex situation that the scientific community is only now
beginning to seriously investigate.
n
They mislead the reader in a number of critical
ways by:
o
failing to acknowledge that the mainstream
scientific community remains highly skeptical of their hypothesis;
o
focusing on the wrong metrics (i.e., sperm, egg
and fertility rather than fecundity);
o
failing to provide essential context to the
reader on the unreliability of much of the scientific evidence they cite;
o
“cherry-picking” the evidence presented and
failing to critically review it and weight it properly;
o
misrepresenting mere correlation as evidence of
causation; and
o
ignoring the critical factors of dose and
potency.
n
The authors recommendations for improving
fertility are not prioritized in any way, are often ill-conceived, impractical,
elitist, and not scientifically justified.
n
Furthermore, the authors either ignore or
misrepresent current industry and regulatory agency practice which leads them
to suggest unsound changes to public policy.
As a consequence of
all of these problems, it should be no surprise that I cannot recommend the
book. Those who may still decide to purchase and read it are urged to do so
with a healthy dose of skepticism – caveat
emptor!
1Although most sources I checked attribute this
quote to Popper, evidently there is some
dispute about its origins.
2see 2017 “Are
your sperm in trouble?”, 2012 “Troubling
chemicals could be poisoning our kids, 2009 “Frogs,
fish and deformities in newborn boys, and 2009 “Chemicals
and Our Health ”.
3The problem with using fertility as a measure is
that there are so many other more important factors that impact it than trace
levels of chemicals in the environment.
For example, as Chivers also noted, the major reason scientists believe
that fertility rates have dropped in developed countries are improvements in
educational level, socioeconomic status, and reproductive rights (e.g., birth
control) of women, and and then the resulting increase in choices they have
about whether and when to have children, and ultimate family size.
4As Ioannidis
notes, many researchers misapply or misinterpret statistical analysis and
consequently underestimate the role of chance in producing the results they
report. Confounding is a common problem
in observational epidemiology studies and is a consequence of a third factor
(e.g., smoking) being corelated with both the exposure agent under
investigation (e.g., occupational exposure to a chemical) and the disease under
study (e.g., lung cancer). If not controlled for in either the design or
analysis, this third factor can mislead the investigator to believing there is
a relationship between the exposure agent and the disease under study. Although investigator bias can indeed unduly
influence all phases of the design, conduct, analysis and reporting of
scientific studies, the use of the term bias in this context refers to the
consequences of errors in measurement of exposures and disease, which actually
occur much more commonly than the public might expect.
5Weight of evidence refers to a systematic
approach that scientists use to evaluate the totality of scientific evidence to
assess if the science supports a particular conclusion. Weight of evidence decisions
do not involve a simple tally of positive and negative studies, but rely on
expert scientific judgment to assess, review and integrate all of the results
to form a meaningful conclusion.
