Exposure science

Exposure science is the study of the contact between humans (and other organisms) and harmful agents within their environment – whether it be chemical, physical, biological, behavioural or mental stressors – with the aim of identifying the causes and preventions of the adverse health effects they result in.^[1][2] This can include exposure within the home, workplace, outdoors or any other environment an individual may encounter.^[3] The term ‘exposure’ is the umbrella term for many different types, ranging from ultraviolet exposure,^[4] exposure to the chemicals in the food we eat,^[5] to exposure to long working hours being the occupational factor most attributable to the burden of disease.^[6]

The need for the field arises from the expansive range of exposures which have resulted in negative health outcomes for humans and other organisms, and mainly focus on the relationship between external exposure, internal exposure and dose.^[2] By tightly integrating the fields of epidemiology, toxicology, biochemistry, environmental science and risk assessment, holistic comprehension of an exposure is achieved to protect human and ecosystem health on an individual, community and global levels.^[1] Though the history of exposure science had an initial slow start, developments have significantly accelerated in the past three decades,^[7] including the beginnings of the formation of the "exposome".^[8] However, there is still much unknown and research in the field is only expanding to cover the increasing amount of identified exposures.

Need

The essentiality of exposure science research extends from the wide range of adverse health outcomes which burden the population. The World Health Organisation predicts that approximately 24% to 40% of the global disease burden is the result of environmental factors, representing the major health burden in developed countries, and indoor smoke from cooking fuels causes 3.8 million deaths every year.^[9] Other morbidities and mortalities as a result of exposure also include cancers (for example, melanoma from UV exposure), autism (linked to high levels of air pollution), Parkinson’s (linked to nitric oxide exposure), and cell damage which causes diabetes, cardiovascular diseases and lung diseases.^[10]

Since research began, there has been many breakthroughs which have improved and protected the health of individuals. An example is the link between UV exposure to the development of all three major forms of skin cancer,^[11] which ultimately led to the development of preventions like sunscreen awareness. Exposure to prenatal infections (for example, influenza, rubella) has been linked increased risks of autism and schizophrenia.^[12] The development of clothing and materials which protect health care workers from infection exposure, and firefighters from heat exposure, has led to increased protection within these occupations.^[13]

However, it is not only human health that exposure science aims to understand and protect, and there are many documented cases where exposure to human activity harms the environment. In 2003, it was discovered that liver damage in fish in Puget Sound (Washington State) was linked to water contamination with polycyclic aromatic hydrocarbons found in coal and gasoline.^[14] Majorly, there has also been the discovery of the depletion of the ozone layer as a result of chlorofluorocarbons and halons found in refrigerators, air conditioners, aircraft halons and aerosol cans.^[15][16] The production of greenhouse gases from sources such as transport and agriculture has been strongly linked to global warming,^[17] which is subsequently causing rising sea-levels and damage to the environments in which many species live within.^[18]

History

One of the earliest accounts of exposure research was conducted by Hippocrates in 400 BC, when he published 'Air, Water, and Places' describing that air, water, food and living quality influenced the prevalence of human disease.^[19] Following well into the late 1900s (AD), there became more and more studies published, such as the link between water contamination and cholera in London in 1855.^[20] However, one of the note worth publications which laid the foundations for the expansion of exposure science into what it has become today was the 'Human Exposure Assessments for Airborne Pollutants: Advances and Opportunities' by the National Research Council.^[21][7] It was the first to "define the core principals of exposure assessment",^[2] and has resulted in increased investments in exposome technologies, growing exposure science programs like HELIX^[22] and the National Exposure Research Laboratory.^[23] The most recent development in exposure science is the shifted focus onto the development of an 'exposome' to match the already underway construction of the complete 'genome'.^[8][24]

Source-to-disease pathway

Understanding the source-to-disease pathway of exposure provides a holistic picture of where the exposure originates and results in harm upon the organism, quoted by Paul Lioy and Kirk Smith (2021) as “exposure science links directly to the sources that might be controlled and to the internal environment of the organisms that are of concern”.^[7][2]

The exposure source can be categorised as exogenous (external) or endogenous (internal) sources. Exogenous sources refer to examples such as radiation, air pollutants, food and social interactions. Endogenous sources refer to examples such as gut microflora, oxidative stress and emotional stress.^[10][25] It is recognised that internal exposure sources can be the result of prior external sources. For example, exposure to vitamin B12 deficient diets can cause hyperhomocysteinemia, which increases oxidative stress within the body leading to the possible development of vascular dementia and stroke.^[26] Identifying the source is essential for determining the factor which has the potential to cause harmful effects upon a human or other organisms. It is also an indicator of which specific fields to incorporate into the studies of their effects. For example, diet related exposures would involve input from nutritionists, however, exposure to radiation would not, involving a chemist instead.^{[citation needed]}

Contact refers to the location or method in which the organism becomes exposed to the source. For example, risk of contact with solar UV exposure only occurs during the daytime, not at night.^[11] A human (or other organism) coming in contact with exposures transitions with different environments, or could alter the dose or frequency of contact with a source.^[1] Establishing contacts allows researchers to identify how they may become avoided or reduced. For example, banning peanut foods (e.g. peanut butter) within schools reduces the chance of a child with a peanut allergy from coming in contact unawares, therefore preventing a reaction.^[27]

Once in contact with the exposure, the route is the pathway in which the exposure reaches areas of the organism where it has the potential to cause damage. Common route examples include inhalation, ingestion, skin absorption or wound contamination.^[7] The route can determine the velocity in which harmful exposure can occur, where inhalation is considered the fastest route of exposure uptake, followed by dermal contact and ingestion.^[28]

The term "dose" is often used interchangeably with the term "exposure", or referred to as exposure dose, target dose, internal dose or external dose to name a few.^[1] Measuring the dose of the exposure required to cause harm is essential for determining the threshold in which the amount of exposure exceeds being harmless and becomes toxic.^[29] This is where the field of exposure science ties directly with toxicology. The dose can also involve the period of time in which the organism is exposed: the more time exposed, the higher the dose and greater potential it exceeds the threshold.^{[citation needed]}

If a dose exceeds it's toxicity threshold, it has the potential to cause some biological effect which results in disease within the organism.^[7] The adverse health effects caused by exposure is the ultimate reason why the field of exposure science emerged.^[1][2]

The 'exposome' concept

The concept of the exposome was first defined by Christopher Paul Wild^[8] as the “life-course environmental exposures (including lifestyle factors), from the prenatal period onwards.” However, similar definitions have been modified from this, including Miller and Jones,^[30] who redefined the exposome as “the cumulative measure of environmental influences and associated biological responses throughout the lifespan, including exposures from the environment, diet, behaviour, and endogenous processes.” The study of the exposome has now been termed ‘exposomics’ in reference to all the technologies used to study the environment, cells and chemicals of an organism.^[10]

The idea stemmed from the pre-existing concept of the ‘genome’, the complete set of genetically encoded instructions which function the body, of which Wild focussed on throughout his career in exposure assessment and cancer genomics. Understanding the genome has led to the ability to predict those who are predisposed to certain chronic diseases.^[8] In his research field, Christopher Wild identifies environmental exposure as the core influencer and mystery of cancer incidence. He concluded the need for the ‘exposome’, like the genome, to map the complete set of environmental exposures a human encounters throughout the course of their lifetime in order to easily prevent and identify sources of exposure-caused chronic diseases, along with target age groups.^[24]

In 2012, Wild continued to extend his description of the exposome and its entailments.^[24] He includes internal bodily processes such as metabolism, hormones, microflora and oxidative stress, external exposures such as radiation, infectious agents and diet, and additionally social, economic and psychological exposures. Increased ease of genotyping and studying polymorphisms saw a major shift to gene-disease related studies in the 1990s and more recently new study designs allow researchers to follow increasing sample sizes.^[8] However, also in 2012, Wild went on to describe the realistic tools and methods one could use to effectively develop the exposome. This included biomarker omics (e.g. genomics, transcriptomics and immunomics), sensor technologies (e.g. using mobile phones to measure physical activity, stress, sleep rhythms) and imaging (for diets, social interactions).^{[citation needed]}

References

1. Council, National Research (2012). Exposure Science in the 21st Century: A Vision and a Strategy. doi:10.17226/13507. ISBN 978-0-309-26468-6. PMID 24901193.
2. R., Lioy, Paul J. Smith, Kirk (2013-01-31). "A Discussion of Exposure Science in the 21st Century: A Vision and a Strategy". Environmental Health Perspectives. National Institute of Environmental Health Sciences. 121 (4): 405–409. doi:10.1289/ehp.1206170. OCLC 841828808. PMC 3620766. PMID 23380895.{{cite journal}}: CS1 maint: multiple names: authors list (link)
3. Dionisio, Kathie L.; Frame, Alicia M.; Goldsmith, Michael-Rock; Wambaugh, John F.; Liddell, Alan; Cathey, Tommy; Smith, Doris; Vail, James; Ernstoff, Alexi S.; Fantke, Peter; Jolliet, Olivier (2015). "Exploring consumer exposure pathways and patterns of use for chemicals in the environment". Toxicology Reports. 2: 228–237. doi:10.1016/j.toxrep.2014.12.009. ISSN 2214-7500. PMC 5598258. PMID 28962356.
4. Lucas, Robyn M (2011). "An Epidemiological Perspective of Ultraviolet Exposure—Public Health Concerns". Eye & Contact Lens: Science & Clinical Practice. 37 (4): 168–175. doi:10.1097/icl.0b013e31821cb0cf. ISSN 1542-2321. PMID 21670693.
5. Landecker, Hannah (2011). "Food as exposure: Nutritional epigenetics and the new metabolism". BioSocieties. 6 (2): 167–194. doi:10.1057/biosoc.2011.1. ISSN 1745-8552. PMC 3500842. PMID 23227106.
6. Pega, Frank; Náfrádi, Bálint; Momen, Natalie C.; Ujita, Yuka; Streicher, Kai N.; Prüss-Üstün, Annette M.; Descatha, Alexis; Driscoll, Tim; Fischer, Frida M.; Godderis, Lode; Kiiver, Hannah M. (2021). "Global, regional, and national burdens of ischemic heart disease and stroke attributable to exposure to long working hours for 194 countries, 2000–2016: A systematic analysis from the WHO/ILO Joint Estimates of the Work-related Burden of Disease and Injury". Environment International. 154: 106595. doi:10.1016/j.envint.2021.106595. ISSN 0160-4120. PMC 8204267. PMID 34011457. S2CID 234793890.
7. Lioy, Paul J. (2010). "Exposure Science: A View of the Past and Milestones for the Future". Environmental Health Perspectives. 118 (8): 1081–1090. doi:10.1289/ehp.0901634. PMC 2920079. PMID 20308034.
8. Wild, Christopher Paul (2005). "Complementing the Genome with an "Exposome": The Outstanding Challenge of Environmental Exposure Measurement in Molecular Epidemiology". Cancer Epidemiology, Biomarkers & Prevention. 14 (8): 1847–1850. doi:10.1158/1055-9965.EPI-05-0456. ISSN 1055-9965. PMID 16103423. S2CID 6446979.
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12. Brown, Alan S. (2012). "Epidemiologic studies of exposure to prenatal infection and risk of schizophrenia and autism". Developmental Neurobiology. 72 (10): 1272–1276. doi:10.1002/dneu.22024. PMC 3435457. PMID 22488761.
13. Dolez, Patricia I.; Vu-Khanh, Toan (2009). "Recent Developments and Needs in Materials Used for Personal Protective Equipment and Their Testing". International Journal of Occupational Safety and Ergonomics. 15 (4): 347–362. doi:10.1080/10803548.2009.11076815. ISSN 1080-3548. PMID 20003769. S2CID 26150582.
14. Myers, Mark S.; Johnson, Lyndal L.; Collier, Tracy K. (2003). "Establishing the Causal Relationship between Polycyclic Aromatic Hydrocarbon (PAH) Exposure and Hepatic Neoplasms and Neoplasia-Related Liver Lesions in English Sole (Pleuronectes vetulus)". Human and Ecological Risk Assessment. 9 (1): 67–94. doi:10.1080/713609853. ISSN 1080-7039. S2CID 84511463.
15. Farman, J. C.; Gardiner, B. G.; Shanklin, J. D. (1985). "Large losses of total ozone in Antarctica reveal seasonal ClOx/NOx interaction". Nature. 315 (6016): 207–210. Bibcode:1985Natur.315..207F. doi:10.1038/315207a0. ISSN 1476-4687. S2CID 4346468.
16. "What Are the Sources of CFCs?". Sciencing. Retrieved 2022-05-27.
17. Arrhenius, Svante (1896). "On the Influence of Carbonic Acid in the Air upon the Temperature of the Ground" (PDF). Journal of Science. 41: 237–276 – via Royal Society of Chemistry.
18. "Is sea level rising?". oceanservice.noaa.gov. Retrieved 2022-05-27.
19. Burnett, C. S. F. (1984). "Abraham Wasserstein: Galen's Commentary on the Hippocratic Treatise Airs, Waters, Places in the Hebrew Translation of Solomon ha-Me'ati. (Proceedings of the Israel Academy of Sciences and Humanities, 6. 3.) Pp. 119. Jerusalem: Israel Academy of Sciences and Humanities, 1982. Paper". The Classical Review. 34 (2): 315. doi:10.1017/S0009840X00104081. ISSN 1464-3561. S2CID 162267457.
20. Snow, John (1855). On the Mode of Communication of Cholera. John Churchill.
21. Council, National Research; Studies, Division on Earth and Life; Sciences, Commission on Life; Pollutants, Committee on Advances in Assessing Human Exposure to Airborne (1991-02-01). Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. National Academies Press. ISBN 978-0-309-04284-0.
22. "Home - HELIX | Building the early life exposome". www.projecthelix.eu. Retrieved 2022-05-27.
23. National Academies of Sciences, Engineering; Studies, Division on Earth and Life; Toxicology, Board on Environmental Studies and; Evaluations, Committee on Incorporating 21st Century Science into Risk-Based (2017-01-05). Advances in Exposure Science. National Academies Press (US).{{cite book}}: CS1 maint: numeric names: authors list (link)
24. Wild, Christopher Paul (2012). "The exposome: from concept to utility". International Journal of Epidemiology. 41 (1): 24–32. doi:10.1093/ije/dyr236. ISSN 0300-5771. PMID 22296988.
25. Rappaport, Stephen M. (2011). "Implications of the exposome for exposure science". Journal of Exposure Science & Environmental Epidemiology. 21 (1): 5–9. doi:10.1038/jes.2010.50. ISSN 1559-064X. PMID 21081972. S2CID 858966.
26. Ueno, Asako; Hamano, Tadanori; Enomoto, Soichi; Shirafuji, Norimichi; Nagata, Miwako; Kimura, Hirohiko; Ikawa, Masamichi; Yamamura, Osamu; Yamanaka, Daiki; Ito, Tatsuhiko; Kimura, Yohei (2022). "Influences of Vitamin B12 Supplementation on Cognition and Homocysteine in Patients with Vitamin B12 Deficiency and Cognitive Impairment". Nutrients. 14 (7): 1494. doi:10.3390/nu14071494. ISSN 2072-6643. PMC 9002374. PMID 35406106.
27. "Minimising the risk of exposure to allergens". education.nsw.gov.au. 2022-03-31. Retrieved 2022-05-27.
28. Systems, National Research Council (US) Commission on Engineering and Technical; Sciences, National Research Council (US) Commission on Life; McKone, Thomas E.; Huey, Beverly M.; Downing, Edward; Duffy, Laura M. (2000). Environmental and Exposure Pathways. National Academies Press (US).
29. Holford, Nicholas H. G.; Sheiner, Lewis B. (1981). "Understanding the Dose-Effect Relationship". Clinical Pharmacokinetics. 6 (6): 429–453. doi:10.2165/00003088-198106060-00002. ISSN 1179-1926. PMID 7032803. S2CID 9337877.
30. Miller, Gary W.; Jones, Dean P. (2014). "The Nature of Nurture: Refining the Definition of the Exposome". Toxicological Sciences. 137 (1): 1–2. doi:10.1093/toxsci/kft251. ISSN 1096-6080. PMC 3871934. PMID 24213143.