18. Parkinson's Disease

  1. David O. Carpenter
  1. Samuel M. Goldman

Published Online: 26 JUL 2013

DOI: 10.1002/9781118679654.ch18

Effects of Persistent and Bioactive Organic Pollutants on Human Health

Effects of Persistent and Bioactive Organic Pollutants on Human Health

How to Cite

Goldman, S. M. (2013) Parkinson's Disease, in Effects of Persistent and Bioactive Organic Pollutants on Human Health (ed D. O. Carpenter), John Wiley & Sons, Inc., Hoboken, NJ, USA. doi: 10.1002/9781118679654.ch18

Editor Information

  1. University at Albany, Institute for Health and the Environment

Publication History

  1. Published Online: 26 JUL 2013
  2. Published Print: 16 AUG 2013

ISBN Information

Print ISBN: 9781118159262

Online ISBN: 9781118679654



  • environmental epidemiology;
  • etiology;
  • mechanistic data;
  • metals;
  • Parkinson's disease (PD;);
  • pathology;
  • pesticide exposure;
  • solvents


Background: Parkinson's disease (PD) is a progressive neurodegenerative disorder of aging that affects 1% of the population over age 50. Although it is a systemic disease, the classic motor features of tremor at rest, slowing of movement, muscular rigidity, and impaired balance result primarily from degeneration of dopaminergic neurons in the substantia nigra. Identified genetic causes comprise only a few percent of PD cases, and several lines of research implicate a major etiologic role for environmental factors.

Objectives: This chapter provides a comprehensive review of PD environmental epidemiology and considers the biological plausibility of toxicant associations in the context of underlying pathological mechanisms.

Discussion: Associations between PD and pesticide exposure have been studied for decades. Evidence is strongest for paraquat, rotenone, and organochlorines such as dieldrin and hexachlorohexane (HCH). The solvents trichloroethylene (TCE) and tetrachloroethylene (PERC) have been associated epidemiologically and produce an animal model that closely recapitulates PD pathology. Mechanistic data implicate polychlorinated biphenyls (PCBs), and epidemiological associations in women are fairly consistent, but much more work is needed. Cellular and animal models also support a possible role for metals in PD etiology. Epidemiological evidence is strongest for lead. However, the most etiologically important exposures may occur perinatally or in early childhood and are difficult to measure.

Conclusions: Epidemiological and basic research strongly implicate a major etiologic role for environmental factors in PD, but only a handful of agents have been consistently associated in human populations. Like most chronic diseases, most PD is caused by multiple factors. Future work should investigate interactions between toxicant exposures and genetic variants that affect their metabolism. The effects of combinations of agents at dosages commonly encountered in human populations should be studied in animal models. Future epidemiological studies in humans should focus on large or pooled populations with well-characterized unbiased exposure estimates and should consider specific agents rather than broad compound classes.