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EBOOKSEPTEMBER 2018

E-Cigarettes: Different But Not SafeThe pressing need to assess the health risks ofe-cigarettes in the face of rising teen use

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Air pollution is a complex mix-ture of gases and particles inthe atmosphere. Air pollutants

are defined as compounds known to be deleterious to human healthand welfare. In the United States, airpollutants are categorised as criteriaand hazardous pollutants. The criteriapollutants generally derive from combustion processes in motor vehicles, electric generating stationsand industrial processes.

Criteria gases include carbon monoxide(CO), sulphur dioxide (SO2), nitrogendioxide (NO2) and ozone (O3); criteriaparticles are denoted by their sizerange, with PM10 and PM2.5 denotingthe mass concentration of particlessmaller than 10 micrometres (millionthsof a metre) or 2.5 micrometres, respec-tively. Hazardous air pollutants aretoxic chemicals, for example, benzeneand arsenic.

In a comprehensive review of theworldwide disease burden of pollu-tion, recently published by The Lancet(“The Lancet Commission on Pollutionand Health”, published online October19, 2017, www.thelancet.com), air pollution was identified as the predominant cause of pollution-asso-ciated morbidity and mortality. Whilethe link between air pollution and respiratory and cardiovascular diseaseis well-established, more recent studieshave raised concerns about thepotential impact of air pollution on

the brain, particularly the developingand the aging brain.

Air pollution and especially traffic-related air pollution have been asso-ciated with increased risk of neuro-degenerative disease, in particular,Alzheimer’s disease (AD) and diverseneurodevelopmental disorders,including autism spectrum disorder(ASD), attention deficit hyperreactivitydisorder (ADHD), learning and intel-lectual disabilities and schizophrenia.These conditions exact a tremendouscost on the affected individual, theirfamilies and society motivating support for research that determineswhether these associations are causaland if so, what components in air pollution are responsible and whatindividual factors (gender, age, nutri-tional status, genetic makeup, etc.)determine whether exposure to airpollution will result in neurological disease?

Researchers employ two complemen-tary disciplines – epidemiology andtoxicology – to study possible linksbetween air pollution and health. Epidemiologic studies use statistics to test the strength of correlationsbetween increased exposure to agiven pollutant and higher incidenceof disease. Epidemiologic studies canidentify associations in the humanpopulation; however, they have a keyweakness, often summarised as “cor-relation does not establish causation”.

Let us take for example living nearheavily trafficked roadways, which hasbeen associated with an increasedincidence of ASD and AD. Is the effectdue to the higher concentration of airpollutants near the roadway or due tothe higher level of noise and vibration,or because housing is less expensivenear busy roadways so people withlower incomes and possibly poor dietlive near these roadways? And even ifair pollution is the cause, which pollu-tant(s) cause the effect?

Another challenge arises from the fact that many neurological diseases,including AD and ASD, result fromcomplex interactions between envi-ronmental factors and genetic suscep-tibilities: The wider the range ofgenetic susceptibilities within a popu-lation, the more challenging it is forepidemiology to identify clear associ-ations between exposure and diseasestate.

Toxicology is a tool for unravellingthese complex questions. To assessthe health impact of air pollution, tox-icologists use models ranging fromcell cultures to laboratory animals andthese can be engineered to expressknown human genetic susceptibilitiesto disease. In contrast to epidemiol-ogy, in toxicology, exposures can becontrolled, and extraneous factorscan be eliminated as variables, suchas noise or diet in the near-roadwayexample above. In this way, toxicolo-

Anthony S. Wexler and Pamela J. Lein from the University of California sharetheir expert views on the impacts of air pollution on the brain

An emerging environmental health concern:Impacts of air pollution on the brain

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gists can determine if air pollutantscause an adverse health effect.

But toxicology faces the challenge ofaccurately mimicking human expo-sures. Think about the complexities ofnear-roadway air pollution, which iscomposed of incomplete combustionexhaust, brake wear, tire wear androad wear as well as derived from amix of vehicles ranging from motor-cycles to heavy duty trucks. At the University of California, Davis, we areaddressing this challenge by locatinganimal exposure facilities adjacent toheavy traffic, so that the animalsbreathe the same mixture as peoplewho live near busy roadways. In addi-tion to assessing neurological outcomesin these animals, we are characteris-ing the chemical composition of theair so future studies can assess thehealth effect of individual componentswithin the polluted air to identify thedisease-causing pollutant(s).

Why are we focusing on the near

roadway example? While regulationspromulgated to reduce emissionshave significantly improved air qualityin cities across North America andWestern Europe, improved air qualityin geographic locations close tosources of air pollution, such as road-ways, power plants and industrialfacilities, have lagged behind. Peopleliving in these locations have a higherincidence of disease, including neuro-logical disease. Since individuals inlower socioeconomic strata are morelikely to reside in more highly pollutedneighbourhoods, the problem ofnear-source air pollution exposure isnot just a public health issue, but alsoan environmental justice issue.

In conclusion, epidemiologic studieshave identified a number of neurolog-ical diseases associated with air pollu-tion. But questions still remain: Is theassociation causal or is there anotherintervening factor that underlies theobserved association? What are thecellular and molecular mechanisms

linking air pollution exposure to neu-ropathology? What components ofthe air pollution are causing neurolog-ical disease – Gases? Particles? Whichones? And what are the sources ofneurotoxic air pollution? This lastquestion is critically importantbecause it is the sources that can becontrolled by regulation. Answers tothese questions, which will requiretoxicology in addition to epidemiology,are required to identify air pollutionemissions control measures thateffectively minimise neuropathologicalrisks.

Pamela J LeinProfessor and Vice-ChairDepartment of Molecular BiosciencesDirector, UC Davis CounterACT Centerof Excellence

Anthony S WexlerDistinguished ProfessorDepartment of Mechanical and AerospaceEngineeringDepartment of Civil and Environmental EngineeringDepartment of Land, Air and Water ResourcesDirector, Air Quality Research Center

University of CaliforniaDavis, CA 95616 USATel: +1 530 752 [email protected] http://www.vetmed.ucdavis.edu/faculty/results.cfm?fid=19369http://www.vetmed.ucdavis.edu/lein-lab/index.cfm

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THE AIR POLLUTION LIFE CYCLE

NaturalEmissions

AnthropogenicEmissions

Atmospheric ProcessingMixingChemical ReactionsPhase Change

Condensation/EvaporationNucleation

Particle Coagulation

HealthEffects

ClimateEffects

Regulation

Gasesand

Particles

Ozone,PM2.5

PM10

ASD, AD

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Worldwide, the frequencyand severity of wildfires areincreasing due to changes in

temperature and precipitation patternsconsistent with climate change andchanges in land use, particularly at therural-urban interface. The fire problemis particularly acute in Northern California, which has experienced asignificant increase in wildfire fre-quency over the past few decades. Inaddition to the risk of injury, loss oflife and destruction of property, thereis increasing appreciation that wild-fires pose significant environmentalhealth threats.

Much of the research on adverse healthimpacts of wildfires has focused onwildfire smoke and recent reviews of this scientific literature concludethere is strong evidence that wildfiresmoke exacerbates respiratory ail-ments, including asthma and chronicobstructive pulmonary disease andcontributes to cardiovascular disease.What is less well understood, however,is the potential impacts of wildfiredebris on human, animal and ecosys-tem health.

Debris from urban wildfires is partic-ularly worrying because these firesinvolve the combustion of buildingmaterials, electronic equipment,chemicals and industrial equipmentthat contain toxic chemicals such asmetals, pesticides and persistentorganic pollutants (POPs).

POPs of concern include the polychlo-rinated biphenyls (PCBs) and poly-brominated diphenyl ethers (PBDEs).PCBs are man-made chemicals thatwere widely produced for diverseindustrial applications beginning inthe 1930s until their production wasbanned in 1979 because of their carcino -genic potential and developmentalneurotoxicity.

PCBs are found in older electricaltransformers, capacitors and light bal-lasts still in use today and in caulkingmaterial, paints and sealants used toconstruct municipal buildings andhomes prior to the 1979 ban. PBDEsare also man-made chemicals thatwere widely used as flame retardantsin various consumer products includ-ing foam, plastics and textiles.

Due to health concerns, the state ofCalifornia began prohibiting the man-ufacture, distribution and processingof flame-retardant products containingpenta- and octa BDEs in 2006. However,human exposure continues becausemany households have products pro-duced prior to the ban. Moreover,PBDEs are not chemically bound tomaterials and therefore, leach out ofhousehold products into the environ-ment. Like PCBs, PBDEs persist in theenvironment and biomagnify up thefood chain.

Pyrolysis results in the release of PCBsand PBDEs into the environment.

Increased PCB concentrations havebeen documented in air masses asso-ciated with fires. The ash from theSeptember 11th 2001 World TradeCenter fire in New York City was foundto contain excessive PBDE levels. Thecombustion of man-made materials,particularly electronic equipment, isalso associated with the mobilisationof metals. For example, ash debrisfrom the California wildfires from 2007contained toxic metals, specifically,arsenic, cadmium, copper and lead, atlevels associated with long-term healtheffects in animals and humans.

Urban wildfires not only release toxicchemicals, but also generate haz-ardous compounds, such as dioxinsand dibenzofurans, which are formedby the combustion of organic matter,such as paper and wood. Once theburning has stopped, re-volatilisedchemicals distribute out of the atmo-sphere onto soils, vegetation and surface water, while non-volatilechemicals are deposited as ash. Theincreased environmental availabilityof these chemicals increases the riskof groundwater contamination, theuptake by plants and ingestion by animals, culminating in increased riskof human exposure for months toyears. Thus, a question of growing con-cern is whether urban wildfires posea significant long-term environmentalhealth risk via chemical contaminationof home-grown produce or animal-derived foods.

Birgit Puschner and Pamela Lein from the University of California, Davis share their expert viewson the impacts of urban wildfire on chemical contamination in small backyard agriculture

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This concern is heightened by lay articles in the New York Times andSan Francisco Chronicle and peer-reviewed publications reportingincreased human exposure to lead(Pb) through consumption of eggsproduced by backyard chickens. Eggs and eggs products are one of the most consumed foods worldwide.In the United States, individuals con-sume an average of 24 grammes ofeggs per day. Backyard chicken own-ership has grown in the United Statesin part because the eggs from back-yard hens are perceived to be healthierthan commercially produced eggs.

However, recent studies have identi-fied concerning levels of Pb in eggsproduced by chickens raised in areaswith significant Pb contamination ofthe soil, usually as the result of theweathering of older buildings with Pb-based paints. The consumption ofone average size 50-60 gramme eggfrom Pb-contaminated environmentcan exceed the safe threshold dose of6µg of Pb per day from all combined

dietary sources. What about PCBs andPBDEs? These are very fat-solublechemicals and egg yolk is rich in lipidsresulting in an average fat content inan egg of 10%. Thus, the potential forsignificant contamination of eggs inregions with increased soil levels ofthese POPs is not unreasonable, assuggested by recent data reportingthe detection of PCBs and PBDEs inmilk from dairy cows of California.

The overwhelming majority of foodsafety research associated with backyard poultry and other home-produced food products has largelyfocused on microbial contamination.Human illness from most foodbornepathogens is limited to transient gas-trointestinal symptoms; in contrast,human exposure to unsafe levels ofPCBs, PBDEs or metals has the poten-tial to cause long-term adverse healtheffects. Currently, urban and backyardfarmers have no way of knowingwhether eggs or other home-grownfood products are contaminated withtoxic chemicals unless they are lab

tested. There is, therefore, an urgentneed to study environmental chemi-cals in home-produced food in geo-graphic regions that have experiencedurban wildfires to assess the potentialfood safety risk and to generate infor-mation needed to inform rational riskmanagement.

In conclusion, the increase in wildfireshas potentially serious long-termhealth consequences for communi-ties and ecosystems. One importantconcern is the generation or releaseof chemicals into the soil and waterenvironment and the risk for chemicalcontamination of home-grown pro-duce, eggs and other animal-derivedfood products. To more accuratelypredict the risk to humans, it will benecessary to obtain data regardingthe actual levels of toxic chemicals ofconcern in the environment beforeand after urban wildfires and to modelthe transfer of these contaminantsthrough the food chain.

Pamela J. LeinProfessor and Vice-ChairDepartment of Molecular BiosciencesDirector, UC Davis CounterACT Centerof [email protected]

Birgit PuschnerProfessor and ChairDepartment of Molecular Biosciences

University of California, DavisTel: +1 530 752 1970http://www.vetmed.ucdavis.edu/lein-lab/

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Wildfire aftermath on Cobb Mountain during the Valley fire in northern California

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212The potential long-term environmental healthconsequences of urban wildfire debris

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402Pesticides: A contributing factor tothe increase in asthma?

Asthma is a chronic inflammatorylung disease, characterised byepisodic and reversible bron-

choconstriction (contraction of thesmooth muscles that line the airways),excessive secretion of mucus in theairways and airway hyperreactivity (an exaggerated reaction of airwaysmooth muscle to contractile stimuli).All of these effects interfere withbreathing.

Worldwide asthma prevalence andseverity has increased markedly overthe past two decades, especially inurban settings. Many hypotheses havebeen proposed to explain the increasedasthma in urban residents, includingexposure to allergens, air pollution,differences in healthcare and stress.However, an environmental factorassociated with agricultural asthmathat is beginning to receive increasedattention in the context of urbanasthma is exposure to organophos-phorus pesticides (OPs).

OPs are the most widely used class ofpesticides worldwide and are appliedextensively in not only agricultural butalso in suburban and urban settingsto control insects. Although residentialuses of OPs are being phased out inthe United States and many Europeancountries, OPs are still used heavily inagricultural, industrial and commercialsettings and OPs are widely detectedin the general human population in all countries in which this has beenassessed.

Occupational exposures associatedwith the production, distribution andapplication of OPs occur primarily viadermal absorption, with more limitedexposure via inhalation. The generalpopulation is exposed to OPs viaingestion of food and water contami-nated with OPs and by dermal andinhalational exposure to pesticidedrift and “overspray”. The latter is notan insignificant source of exposure asextensive OP contamination has beendocumented in the air, homes andurine from pregnant women and children living in communities nearagricultural fields sprayed with OPs

OPs inhibit the enzyme acetylcholine -sterase, which functions to inactivatethe neurotransmitter acetylcholine.Acetylcholinesterase inhibition signif-icantly increases acetylcholine levelsat the synaptic junction betweennerves that secrete acetylcholine andtheir target tissues, causing excessivestimulation of target tissues.

Acetylcholinesterase activity is func-tionally important in not only insects,but also humans. It is well establishedthat OPs cause neurotoxicity in humansby inhibiting this enzyme, a medicalcondition referred to as the choliner-gic crisis. Acute exposures to OPs thatinhibit acetylcholinesterase by morethan 80-90% of control levels cancause death in humans, typically byinhibiting the respiratory centres inthe brain that control breathing. Thus,many regulatory agencies have iden-

tified safe levels of OPs as those thatdo not inhibit acetylcholinesterase.

Case reports published in the 1960’sprovided the first indication that exposures to OPs at levels that do notcause cholinergic crisis may triggerasthma in adults. Subsequent cross-sectional studies of farmers and theirfamilies, farmworkers and commer-cial pesticide applicators in multiplecountries around the world providedfurther evidence that occupationalexposures to OP pesticides are asso-ciated with adult-onset asthma.

More recent epidemiologic data suggest that not only occupationalexposures, but also exposures to environmentally relevant levels ofOPs, such as might be experienced bythe general public, are associated withincreased risk of asthma and asthmaticsymptoms in adults and adolescents.OP-induced asthma may not be limitedto these age groups, as indicated byemerging data from the Center for theHealth Assessment of Mothers andChildren of Salinas (CHAMACOS), thelongest-running longitudinal birthcohort study of pesticide effects onchildren’s health, which has beenstudying children in a farmworkercommunity in the Salinas Valley ofnorthern California. Data from theCHAMACOS study suggests that OPexposures during pregnancy and thefirst year of life, as determined byanalysis of urinary OP metabolites inpregnant women and their infants,

Pamela J. Lein at the University of California, Davis discusses the evidencesuggesting that pesticides are risk factors for asthma

Pesticides: A contributing factor to the increase in asthma?

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are associated with respiratory symp-toms in children at five and sevenyears of age.

While systematic reviews of the published epidemiologic literaturegenerally support an associationbetween OP pesticide exposure andasthma, it is difficult to establish acause-effect relationship based onhuman data. This is due in large partto the fact that it is extremely chal-lenging to accurately quantify OPexposure in humans. Thus, studies inanimal models are critical for deter-mining whether OPs are causallylinked to asthma. The animal studiespublished to date support the hypoth-esis that OPs directly cause airwayhyperreactivity, a key symptom ofasthma.

Importantly, OP-induced airwayhyperreactivity is observed at levelsthat do not inhibit acetylcholine -sterase. Several different OPs, includingchlorpyrifos, parathion and diazinon,can induce airway hyperreactivity inguinea pigs following subcutaneousinjection, a route of exposure thatmimics dermal exposure in humans.In contrast, pyrethroids, a class of pesticides structurally and mechanis-tically distinct from OPs, do not induceairway hyperreactivity in guinea pigs,suggesting that the airway responseto OPs is not a generalised property ofall pesticides.

Interestingly, the effect of OPs onairway hyperreactivity was not evidentimmediately after exposure, but ratherwere manifest 24 hours later and

persisted for at least seven days aftera single injection of the OP. Furtherstudies in the guinea pig model suggestthat OPs cause airway hyperreactivityby interfering with neural mechanismsthat normally function to limit therelease of acetylcholine from airwaynerves onto airway smooth muscle.This effectively increases the amountof acetylcholine available to causecontraction of the airway smoothmuscle.

How OPs cause dysfunction of airwaynerves remains an outstanding question, although preliminary datasuggest that the mechanism may varydepending on the allergic status of theindividual. Answering this questionwill be critical for identifying suscepti-ble subpopulations and for designingmore effective therapeutic interven-tions for preventing or reversing OP-induced airway hyperreactivity.More immediately, these findingsraise significant questions regardingthe use of acetylcholinesterase activity as a point of departure for regulatory action. Furthermore, thesefindings suggest the possibility thatthe increased prevalence of asthma isrelated less to the insects that we livewith than to the chemicals we use tokill them.

Pamela J. LeinProfessorUniversity of California, DavisTel: +1 530 752 [email protected]://www.vetmed.ucdavis.edu/lein-lab/

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Farm worker spraying pesticide treatment on fruit garden

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228Polychlorinated biphenyls (PCBs): A persistent environmental health problem

Polychlorinated biphenyls (PCBs)are a family of synthetic chem-icals that were produced in

large quantities for industrial andcommercial applications beginning inthe late 1920s through the late 1970s.PCB mixtures were synthesised globally and identified under severaltrade names, including Aroclor®(United States and United Kingdom),Clophen® (Germany), Phenclor®(France) and Kanechlor® ( Japan).Chemically, PCBs are biphenyls withvariable chlorine atoms substituted for the hydrogen atoms in the benzenerings. There are 209 possible PCBcompounds – each of which isreferred to as a congener – that arenamed according to the number andposition of chlorine substitutions (i.e.,lower-chlorinated congeners havelower number designations andhigher-chlorinated congeners thathave higher number designations).

While concern regarding adversehealth outcomes associated withoccupational exposures to PCBs aroseas early as the 1930s, by the 1960s and1970s there was significant alarm aboutthe human health risks of PCBs in theenvironment. The manufacturing, useand disposal of PCBs had resulted inwidespread PCB contamination of air,water and soil, and because PCBs arehighly resistant to degradation, theyhad accumulated in the human foodchain and were readily detected inhuman tissues, including breast milk.

These observations, coupled withemerging data linking environmentalPCB levels to increased cancer risk inhumans and animal models, impelledthe United States Congress to insti-tute a ban on PCB production in 1979.This was followed by a global ban onthe production and use of PCBs by theStockholm Convention on PersistentOrganic Pollutants in 2001.

In the decades following the ban onPCB production, environmental PCBlevels decreased significantly. Duringthis time, basic research scientistsidentified the biological mechanismsby which PCBs cause cancer and regulatory scientists established “safe”exposure levels for PCBs in the envi-ronment and human food suppliesbased on attributable cancer risk. It

was widely believed that the PCBproblem was solved and that furtherresearch on PCBs was not warranted.However, emerging research on PCBsover the past decade has revealed anumber of unexpected findings thatsuggest the mainstream understand-ing of PCB exposures and PCB toxicitymay be too limited and that PCB reg-ulations focused on cancer outcomesmay not be protective of vulnerablepopulations.

One surprise from current research isthat while environmental levels ofPCBs are decreasing globally, levelshave stabilised or may be increasingin some geographic regions. Oneexplanation is the accelerated releaseof “legacy” PCBs from ageing products.For example, higher than expected

Carolyn R. Klocke, Postdoctoral Scholar and Pamela J. Lein, Professorat University of California, Davis both argue that polychlorinatedbiphenyls (PCBs) are a persistent environmental health problem today

Polychlorinated biphenyls (PCBs): A persistent environmental health problem

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PCB Cleanup site at Sheboygan Falls, Wisconsin, United States, circa 1990

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levels of PCBs in the air over the cityof Chicago are thought to be due inpart to the release of PCBs fromageing paints and caulking materialsused to construct municipal buildingsduring the era when PCBs were inten-tionally added to these constructionmaterials. The release of legacy PCBsfrom paints and caulking materialsmay also explain why PCB levels in theindoor air of elementary schools inthe United States exceed the 2009public health guidelines set by theUnited States Environmental Protec-tion Agency. Additionally, novel PCBsthat were not part of the originalindustrial mixtures have beendetected in the environment and inhuman tissues. The toxic potential ofmost of these contemporary PCBs,many of which are lower chlorinatedcongeners, is largely unknown.

Historically, consumption of contami-nated food was thought to be the primary source of PCB exposure inhumans, with fish, meat and dairyproducts comprising the main dietarysources of PCBs. However, recentstudies documenting PCB contaminantsin the air of major cities and indoor airof municipal buildings, includingschools, suggest that inhalation maybe a significant and underappreciatedsource of human exposure. Whilesources of airborne PCBs, which includeboth legacy PCBs as well as the lowerchlorinated contemporary PCBs, arenot yet completely understood, somestudies have demonstrated that PCBscan be unintentionally producedduring the synthesis of yellow andgreen paint pigments. Once dried,volatile PCBs can be released into theair (a phenomenon also referred to as“off-gassing”) to be inhaled by

humans. Whether the toxic effects ofPCB are different if they are inhaledfrom the air vs. ingested with foodremains to be determined.

Another evolution in our understandingof the environmental health impactsof PCBs is the realisation that thedeveloping brain is a vulnerable targetof PCBs. PCBs interfere with thegrowth and maturation of neurons inthe developing brain, which shifts thedevelopmental trajectory of the brainin a manner that disrupts normal patterns of connections betweenbrain regions. The magnitude of thiseffect differs depending on the specific PCB congener involved andwhether it is a higher- or lower-chlori-nated congener. Interestingly, apathological change that is commonto many neurodevelopmental disor-ders, including autism and attentiondeficit hyperactivity disorder (ADHD),is altered connectivity in the brain, andrecent studies report that elevatedmaternal PCB levels are associatedwith increased risk of having a childwith autism or ADHD.

The recent discovery of PCB contami-nation in the indoor and outdoor airhas also raised concern regarding theeffects of exposure to airborne PCBson the developing lung. Lung develop-ment continues long after birth, sothere is the possibility that inhalationof PCBs interferes with lung develop-ment and growth. Since PCBs areknown to interfere with neuronaldevelopment, it is hypothesized thatthe inhalation of airborne PCBs mayinterfere with innervation of the lung,resulting in increased airway hyperre-activity, a hallmark characteristic ofasthma. It has been hypothesized that

airborne PCBs contribute to the unex-plained and perplexing increase inchildhood asthma since the 1960s.

Collectively, epidemiologic studiesand experimental data from animalmodels suggest that further investiga-tion of PCBs is warranted to under-stand how the changing patterns ofPCB exposure are contributing to non-cancer outcomes, specificallyneurodevelopmental disorders andpotentially pediatric asthma. Such workis required to ensure that regulatorypolicies targeting PCBs are protectiveof the most vulnerable members ofsociety.

Carolyn R. KlockePostdoctoral ScholarUniversity of California, [email protected]/in/carolyn-klocke

Pamela J. LeinProfessorUniversity of California, DavisTel: +1 530 752 [email protected]/lein-lab/

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Obesity is a metabolic diseasecharacterised by excessivebody fat that is defined

clinically as having a body mass index(BMI) over 30. For the first time inhuman history, the number of obeseand overweight people is greater thanthe number of those who are under-weight. An estimated 1/3 of the world’spopulation currently meet the clinicaldefinition of obese, and it is predictedthat approximately half the world’spopulation will be obese by 2030.

Obesity is a major risk factor fornumerous life-threatening diseases,including cardiovascular disease,cancer, and Type 2 diabetes, and in2014, the global economic burden ofobesity was estimated to be $2 trillion.Given the significant health and economic impacts of obesity, there isan urgent need to identify the risk factors involved in the development ofobesity. While caloric excess andsedentary lifestyle are classically iden-tified as the main drivers of obesity,these two factors do not explain therecent dramatic rise in the global incidence of obesity.

Factors that are receiving increasedscrutiny as potential risk factors forobesity are chemicals that interferewith the action of hormones that regulate metabolism and weight gain.These chemicals, which are referredto as “environmental obesogens”, are

thought to promote obesity by inter-fering with metabolic homeostasis.

In support of the obesogen hypothe-sis, several human studies havedemonstrated a positive associationbetween exposure to environmentalchemicals and obesity. For example,increased levels of dichlorodiphenyl-trichloroethane (DDT), a pesticide oncewidely used to control mosquitoes,have been linked to higher BMI in both children and adults in multiplepopulations around the world. Morerecently, maternal smoking or expo-sure to near roadway air pollutionhave been reported to increase therisk of childhood obesity.

While human studies are essential forassessing the feasibility of the envi-ronmental obesogen hypothesis, theydo not establish that exposure to DDT,air pollutants, or other environmentalchemicals, actually cause obesity. Thisis because it is difficult to tease outwhether other factors that coincidewith environmental exposure, such associoeconomic stressors, may be theactual cause. However, studies of laboratory animals maintained in acontrolled environment on a fixed diethave confirmed that at least someenvironmental chemicals can increasethe risk of obesity.

Studies of animal and cell culturemodels are also providing insight as to

how environmental chemicals promotean obese phenotype. For example,environmental chemicals can increasefat storage capacity by increasing thenumber and/or size of fat cells, knownas adipocytes. Cell culture experimentssuggest that the industrial chemicaltributyltin (TBT) increases the numberof adipocytes by activating a receptorthat promotes the differentiation ofstem cells into adipocytes.

“Obesity is a global epidemic thataffects adults, children and infants,and the rising incidence of obesity andits related diseases shows no signs oflevelling off.”

Consistent with these observations,experimental animal models exposedto environmentally relevant concentra-tions of TBT during development haveincreased fat accumulation in adiposetissues and the liver compared to con-trol animals. Of concern, these studiessuggest that the obesogenic effect ofTBT is transgenerational, meaning thatTBT may influence obesity risk in notonly the individual exposed duringdevelopment but also in the childrenand even grandchildren of the exposedindividual.

Obesogens have also been shown toaffect adipocyte function. Healthyadipocytes not only store energy butalso produce hormones that signalthroughout the body to control

A group of experts from the University of California, Davis and the Universityof Southern California explain the extent to which environmental chemicals arecontributing to the obesity epidemic

Are environmental chemicalscontributing to the obesity epidemic?

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appetite and energy balance. Air pollu-tants can interfere with both of theseprocesses, increasing the body’s abilityto store energy while also decreasingthe production of hormones importantfor metabolic health. The body alsocontains a special type of adiposetissue called brown adipose, whichburns energy to create heat to main-tain body temperature. This process isknown as thermogenesis, anddecreased thermogenesis has beenlinked to obesity in humans. Develop-mental exposure to DDT hinders thermogenesis in mice and decreasesthe expression of genes involved inburning energy.

The hypothalamus is a region of thebrain that monitors and responds tochanges in the body’s hormonal andnutritional status to maintain metabolichomeostasis, and disruption ofhypothalamic function can lead toobese phenotypes in animal models.Recent studies in mice have shown thatexposure to air pollutants increasesinflammation in the hypothalamus,which can interfere with hypothalamicfunction, and this effect coincides withincreased body weight. Another animalstudy of the obesogenic effects of air

pollution linked increased obesity withdecreased expression of hormonereceptors involved in appetite regula-tion. Whether environmental chemicalsalter the hypothalamus in other waysremains a critical data gap.

Obesity is a global epidemic thataffects adults, children and infants,and the rising incidence of obesityand its related diseases shows nosigns of levelling off. These alarmingtrends warrant research focused onunderstanding the relative contribu-tion of environmental chemicals tothe development of obesity, especiallysince exposures to environmentalchemicals are modifiable risks. How-ever, an effective public health strat-egy requires determining which of thetens of thousands of chemicals in thehuman environment have obesogenicactivity. It may be possible to addressthis problem by leveraging cell culturemodels that express receptors thatdrive adipocyte differentiation or areimplicated in controlling feedingbehaviours. Chemicals found to acti-vate these receptors in cell culture atenvironmentally relevant concentra-tions could then be studied in preclin-ical models to confirm obesogenic

potential at the organism level. Inaddition, it will be important to edu-cate the public – especially pregnantwomen – as to the effects of environ-mental exposures on the disease riskin their child. Given the increasing evidence linking chemical exposure inutero to increased risk of obesity, itwill be important to educate parentson the approaches for mitigating orreducing their exposure to suspectedenvironmental obesogens before,during and after pregnancy, with thegoal of reducing the risk of obesity intheir children.

References

1 Heindel, J. J. et al. Metabolism disrupting chemicals and

metabolic disorders. Reprod. Toxicol. 68, 3-33, doi:10.1016/j.re-

protox.2016.10.001 (2017).

2 Janesick, A. S. & Blumberg, B. Obesogens: an emerging threat to

public health. Am. J. Obstet. Gynecol. 214, 559-565,

doi:10.1016/j.ajog.2016.01.182 (2016).

Carolyn R. Klocke, PhDPostdoctoral ScholarUniversity of California, [email protected]/in/carolyn-klocke

Sunjay Sethi, PhDPostdoctoral ScholarUniversity of Southern CaliforniaTel: +1 323 671 [email protected]

Pamela J. Lein, PhDProfessorUniversity of California, DavisTel: +1 530 752 [email protected]/lein-lab/www.twitter.com/UCDATEHS1

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316Are environmental chemicals contributingto the obesity epidemic?

ISSUE 21 • JANUARY 2019

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