Recommended Reading

We have selected papers which are available for free. They are only a tiny selection of research into some of the health problems in a vast research literature – they should serve as an introduction to the serious science rather than a definitive guide to the issues.

Where possible, we have linked directly to the study. Otherwise, the links will take you to PubMed, the primary on-line database for environmental health research. From there you can download the studies (the link is usually in the top-right corner of the page.) On this page:

  • Cancer
  • Reproductive health  (fertility, age of puberty, healthy pregnancy etc.)
  • Psychological development (ADHD, autism, intelligence etc.)
  • Obesity and diabetes
  • Endocrine disrupting chemicals
  • Interpreting evidence (a major challenge in developing chemicals policy)
  • Green chemistry and safer substitutes for harmful substances


For a time it was thought that genes, not the environment, was the primary cause of cancer. Now it seems that most cancers are attributable to environmental causes – but be warned, for scientists studying these issues “environmental” simply means “non-genetic”.

There is still a healthy debate over what proportion of cancers are caused by pollution and their relative importance next to lifestyle choices. The US President’s Cancer Panel report is particularly worth reading for a a detailed presentation of why chemicals are increasingly of interest as potential causes of cancer.

American Cancer Society perspectives on environmental factors and cancer.  Fontham et al. CA Cancer J Clin, 2009; 59(6):343-51. An overview of the ACS’s approach to the prevention of cancer associated with such toxic pollutants in the context of its mission and priorities with respect to cancer prevention.

Environmental and heritable factors in the causation of cancer–analyses of cohorts of twins from Sweden, Denmark, and Finland.  Lichtenstein et al. N Engl J Med. 2000 Jul 13;343(2):78-85. PubMed PMID: 10891514. Inherited genetic factors make a minor contribution to susceptibility to most types of neoplasms. This finding indicates that the environment has the principal role in causing sporadic cancer.

Environmental and occupational causes of cancer: new evidence 2005-2007.  Clapp RW, Jacobs MM, Loechler EL. Rev Environ Health. 2008 Jan-Mar;23(1):1-37. Review. PubMed PMID: 18557596; PubMed Central PMCID: PMC2791455. An argument for a new cancer prevention paradigm which addresses multiple interacting factors rather than prioritising isolated, fractional causes. The new paradigm demands limiting exposures to avoidable environmental and occupational carcinogens in combination with additional important risk factors such as diet and lifestyle.

*Reducing Environmental Cancer Risk: What We Can Do Now. [PDF] The President’s Cancer Panel (2010). The Panel was particularly concerned to find that the true burden of environmentally induced cancer has been grossly underestimated. With nearly 80,000 chemicals on the market in the United States, many of which are used by millions of Americans in their daily lives and are un- or understudied and largely unregulated, exposure to potential environmental carcinogens is widespread.

Reproductive health

Concerns around chemicals and reproductive health focus on fertility, healthy development of the sex organs (rather than, for example, being born with an undescended testicle) and healthy pregnancy, so the foetus develops properly and is not impaired either physiologically or mentally.

Phthalates, used to soften plastics, have been of particular interest to researchers because of their ability to block the action of testosterone, which affects not only fertility in men but can make gender-specific alterations to the brain of the developing foetus.

PBDE concentrations in women’s serum and fecundability. Harley et al. Environ Health Perspect. 2010 May;118(5):699-704. This study was designed to determine whether maternal concentrations of brominated flame retardants in serum collected during pregnancy are associated with time to pregnancy and menstrual cycle characteristics.

Environmental/lifestyle effects on spermatogenesis. Sharpe RM. Philos Trans R Soc Lond B Biol Sci. 2010 May 27;365(1546):1697-712. This review assesses potential causes involving adverse effects on testis development in perinatal life (primarily effects on Sertoli cell number), which are probably irreversible, or effects on the process of spermatogenesis in adulthood, which are probably mainly reversible.

Environmental anti-androgens and male reproductive health: focus on phthalates and testicular dysgenesis syndrome. Fisher JS. Reproduction. 2004 Mar;127(3):305-15. This review aims to give a brief overview of the issues surrounding the perceived decline in human male reproductive health and the importance of the hormonal environment for the development of the testis and reproductive tract.

Prenatal exposure to phthalates and infant development at 6 months: prospective Mothers and Children’s Environmental Health (MOCEH) study. Kim et al. Environ Health Perspect. 2011 Oct;119(10):1495-500. The results of this study suggest that prenatal exposure to phthalates may depress the Mental and Psychomotor Developmental Indices of infants, particularly males, at 6 months.

Psychological development

Chemicals can affect the normal psychological development of the child, by permanently altering the development of the brain or by affecting brain signalling. Measuring the effects can be difficult (a small drop in IQ may not affect an individual much, but over a population can be highly socially significant). Interpreting the evidence can also be tricky, as shown below by the commentary on the US FDA’s evaluation of food colouring and the recent discovery that autism may be far more environmentally-influenced than previously thought.

A strategy for comparing the contributions of environmental chemicals and other risk factors to neurodevelopment of children. Bellinger DC. Environ Health Perspect. 2012 Apr;120(4):501-7. This review compares the relative impact of different environmental risk factors with effects of other risk factors (such as brain injury and pre-term birth) to find that pollutants make startlingly substantial contributions to neurodevelopmental morbidity. Synopisis here.

Synthetic food colors and neurobehavioral hazards: the view from environmental health research. Weiss B. Environ Health Perspect. 2012 Jan;120(1):1-5. A detailed commentary on weaknesses in the FDA assessment of the safety of food colourants, focusing in particular on the FDA’s interpretation of a large 2007 study as inconclusive.

Genetic heritability and shared environmental factors among twin pairs with autism. Hallmayer et al. Arch Gen Psychiatry. 2011 Nov;68(11):1095-102. doi: 10.1001/archgenpsychiatry.2011.76.  Autism is considered the most heritable of neurodevelopmental disorders. This study, quantifying estimates of genetic heritability of autism, finds moderate genetic heritability and a substantial shared twin environmental component.

Endocrine disruptors and childhood social impairment. Miodovnik et al.Neurotoxicology. 2011 Mar;32(2):261-7.  In this study, higher concentrations of BPA or certain phthalates in urine are associated with more atypical social behaviors. The phthalates found in fragrances and personal care products are most strongly associated with these behaviors.

Obesity and diabetes

Chemicals probably can’t make you fat, but there is evidence they can subtly adjust metabolic balance in the body in such a way as to make it more likely that an individual will gain weight (after all, it does not take much of a calorie imbalance to result in substantial weight gain over a period of several years).

There is also evidence that, while obesity has been identified as a major risk factor for diabetes, that it may not be sufficient to cause diabetes, but that background levels of POPs combine with obesity to cause diabetes.

Obesogens, stem cells and the developmental programming of obesity. Janesick & Blumberg. Int J Androl. 2012 Jun;35(3):437-48. Humans exposed to obesogenic chemicals during sensitive windows of development might be pre-programmed to store increased amounts of fat, exacerbating the deleterious effects of poor diet and inadequate exercise.

Environmental estrogens and obesity. Newbold et al. Mol Cell Endocrinol. 2009 May 25;304(1-2):84-9. A study strongly suggesting that DES induces a range of changes which set a mouse’s metabolism to conserve energy, as if it were living in a low-resource environment, thereby predisposing it towards obesity.

Environmental contaminants as risk factors for developing diabetes. Carpenter DO. Rev Environ Health. 2008 Jan-Mar;23(1):59-74. It seems that obese persons who do not have elevated POPs are not at elevated risk of diabetes, suggesting that the POPs rather than the obesity per se is responsible for the association.

Low dose of some persistent organic pollutants predicts type 2 diabetes: a nested case-control study. Lee et al. Environ Health Perspect. 2010 Sep;118(9):1235-42. One of three studies confirming that higher levels of POPs in obese people causes type-2 diabetes, rather than the other way around.

Endocrine disrupting chemicals

The Endocrine Society has published two extensive reviews of the evidence supporting endocrine disruption and the appropriate regulatory steps required for controlling the risk they pose to population health.

Endocrine-disrupting chemicals: an Endocrine Society scientific statement. Diamanti-Kandarakis et al.  Endocr Rev, 2009; 30(4):293-342.

Endocrine-Disrupting Chemicals and Public Health Protection: A Statement of Principles from The Endocrine Society. Zoeller et al. Endocrinology. 2012 Jun 25.

Hormones and endocrine-disrupting chemicals: low-dose effects and nonmonotonic dose responses. Vandenberg et al. Endocr Rev. 2012 Jun;33(3):378-455. A review illustrating that nonmonotonic responses and low-dose effects are remarkably common in studies of natural hormones and EDCs.

Interpreting evidence and developing policy

One of the newest and most interesting developments in chemicals policy is, in fact, chemicals policy itself. The majority of research into how chemicals affect health has only been carried out in the last decade, while REACH is the first international, systematic attempt to regulate chemicals in a pro-active way.

Marrying new research of uncertain significance to a new regulatory framework, in the midst of the hyper-acceleration of exchange of information brought about by the internet,  is challenging, controversial, and requires a much more sophisticated understanding of the interplay between science and policy. It demands transparency above all else.

How strong is the evidence of a link between environmental chemicals and adverse effects on human reproductive health? Sharpe RM, Irvine DS. BMJ. 2004 Feb 21;328(7437):447-51. New understanding and emerging results are reshaping our thinking of how the environment is a determinant of disease, as is the recognition that establishing cause and effect for environmental chemical exposures is a daunting task.

US National Institute for Environmental Health Sciences’ New Strategic Plan. Birnbaum LS. Environ Health Perspect. 2012 Aug;120(8):a298. The Director of the US National Institute for Environmental Health Sciences outlines how her organisation is moving on from “the antiquated idea that the dose makes the poison”, stating that “low-dose research must go hand in hand with [a] life-span approach”.

Risk to all or none? A comparative analysis of controversies in the health risk assessment of Bisphenol A. Beronius A, Rudén C, Håkansson H, Hanberg A. Reprod Toxicol. 2010 Apr;29(2):132-46. Differences in conclusions were mainly influenced by the evaluation of low-dose effects and the uncertainties surrounding the significance of these data for health risk assessment. The results illustrate the impact of differences in risk assessment policy and expert judgment on the risk assessment process and highlight the importance of transparency in this process.

Understanding the mismatch between the demands of risk assessment and practice of scientists–the case of Deca-BDE. Alcock RE, Macgillivray BH, Busby JS. Environ Int. 2011 Jan;37(1):216-25. There is a sustained gap between the aims and practices of research scientists and those of risk management. A more rigorous scientific process that treats different elements of input data as discrete pieces of evidence is needed to ensure that science rather than politics will always define chemical safety.

Green chemistry and safer substitutes

Economy of resources and process efficiencies are important, but when it comes to green chemistry CPES is primarily interested in the development of compounds with a strong pedigree of environmental safety – that are not toxic, persistent, bioaccumulative, carcinogenic, reprotoxic, or likely to cause other harm of an equivalent level of concern.

Much work needs to be done here, as illustrated by there being only one open-access paper discussing how green chemistry can advance environmental health.

Toward a new U.S. chemicals policy: rebuilding the foundation to advance new science, green chemistry, and environmental health. Wilson & Schwartzman. Environ Health Perspect. 2009 Aug;117(8):1202-9. A description of fundamental weaknesses in U.S. chemicals policy, present principles of chemicals policy reform, and articulate interdisciplinary research questions that should be addressed.

About CPES

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