References and provenance¶
The exposure examples combine selected material from ALS_exposures_mechanism_prevention_standards.xlsx, prepared 10 November 2026, with the primary studies and official data documentation linked below. The workbook describes itself as exploratory and not peer reviewed. The selection is an educational guide, not a systematic review or formal evidence grading exercise.
Lead studies¶
R1. Fang F, Kwee LC, Allen KD, et al. Association between blood lead and the risk of amyotrophic lateral sclerosis. American Journal of Epidemiology. 2010;171(10):1126–1133. Full text. Case-control evidence using blood lead and bone-turnover measures. Workbook reference 6.
R2. Kamel F, Umbach DM, Stallone L, et al. Association of lead exposure with survival in amyotrophic lateral sclerosis. Environmental Health Perspectives. 2008. DOI: 10.1289/ehp.11193. PubMed. A prognosis study among people with ALS; it does not establish a beneficial effect of lead. Workbook reference 7.
Pesticide study¶
R3. Kamel F, Umbach DM, Bedlack RS, et al. Pesticide exposure and amyotrophic lateral sclerosis. Neurotoxicology. 2012;33(3):457–462. DOI: 10.1016/j.neuro.2012.04.001. Full text. Includes original Agricultural Health Study analyses and a meta-analysis. The example uses its original cohort findings. Additional source for the pesticide example.
Air-pollution studies¶
R4. Pedde M, Adar SD, D'Souza J, Feldman EL, Goutman SA. Air pollution and disease progression in a University of Michigan amyotrophic lateral sclerosis cohort. Environmental Research. 2026;289:123398. DOI: 10.1016/j.envres.2025.123398. PubMed. Repeated ALSFRS-R measurements and modeled residential pollution. Workbook reference 40.
R5. Chalitsios CV, Rudolf O, Gao J, Turner MR, Thompson AG. Long-term exposure to ambient air pollution and incident amyotrophic lateral sclerosis: a prospective cohort analysis of the UK Biobank. Neurology. 2026;106(8):e214858. DOI: 10.1212/WNL.0000000000214858. PubMed. No association with incident ALS for the evaluated pollutants. Workbook reference 43.
Solvent study¶
R6. Malek AM, Barchowsky A, Bowser R, et al. Exposure to hazardous air pollutants and the risk of amyotrophic lateral sclerosis. Environmental Pollution. 2015;197:181–186. DOI: 10.1016/j.envpol.2014.12.010. PubMed. A case-control study with 51 matched pairs and modeled aromatic-solvent exposure. Workbook reference 42.
Bloom mapping study¶
R7. Torbick N, Ziniti B, Stommel E, et al. Assessing cyanobacterial harmful algal blooms as risk factors for amyotrophic lateral sclerosis. Neurotoxicity Research. 2018. DOI: 10.1007/s12640-017-9740-y. Full text. A spatial study combining satellite-derived phycocyanin estimates and ALS geography; individual toxin dose was not measured. Additional source for the bloom example.
BMAA laboratory studies¶
R8. Dunlop RA, Cox PA, Banack SA, Rodgers KJ. The non-protein amino acid BMAA is misincorporated into human proteins in place of L-serine causing protein misfolding and aggregation. PLOS ONE. 2013;8(9):e75376. Article. Laboratory evidence supporting the proposed mechanism. Workbook reference 17.
R9. van Onselen R, Downing S, Kemp G, Downing T. Investigating β-N-methylamino-L-alanine misincorporation in human cell cultures: a comparative study with known amino acid analogues. Toxins. 2017;9(12):400. DOI: 10.3390/toxins9120400. Full text. Laboratory findings that did not support the proposed incorporation mechanism. Additional source presenting conflicting evidence.
Formaldehyde studies¶
R10. Weisskopf MG, Morozova N, O'Reilly EJ, et al. Prospective study of chemical exposures and amyotrophic lateral sclerosis. Journal of Neurology, Neurosurgery & Psychiatry. 2009;80(5):558–561. DOI: 10.1136/jnnp.2008.156976. PubMed. Prospective study of reported chemical exposures and ALS mortality. Workbook reference 34.
R11. Pinkerton LE, Hein MJ, Meyers A, Kamel F. Assessment of ALS mortality in a cohort of formaldehyde-exposed garment workers. Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration. 2013. Full text. Occupational cohort findings that did not support an association. Additional source for the formaldehyde example.
Workbook selection¶
Row numbers below refer to the Excel worksheet rows, including its notice and header rows. Numbered items refer to the workbook's exposure labels.
| Site example | Exposures sheet | Workbook material used |
|---|---|---|
| Lead | Row 3, item 1 | Geographic assessment, biomonitoring and separate risk/survival questions |
| Pesticides and herbicides | Rows 8–9, items 6–7 | Chemical-specific use data and occupational history |
| Air pollution | Row 13, item 11 | Repeated residential estimates, progression and incidence studies |
| Solvents and industrial sites | Rows 4 and 11, items 2 and 9 | Contaminant-specific site linkage and exposure pathways |
| Cyanobacterial blooms | Rows 5–7, items 3–5 | Distinction between bloom events, organisms and chemicals |
| Occupational formaldehyde | Row 12, item 10 | Work history and limits of residential estimates |
The overview also draws on the workbook's Standards coverage and Standards summary sheets to illustrate the roles of ontologies, clinical measurement codes and the OMOP GIS extension. Proposed assay, omics and intervention ideas remain hypotheses. This section does not reproduce the full workbook or assign validated status to its evidence tags, candidate genes or adverse outcome pathway mappings.
Official data and implementation documentation is linked alongside each source on Data sources and linkage limits and Environmental mapping. References and documentation for these selected examples were checked on 12 November 2026; this was not an audit of every workbook entry or every page in GIS Commons.