Pesticide Exposure and Human Health (Part 2)DONNA L. HOUGHTON, Ph.D., SYNGENTA CROP PROTECTION CAN. INC.

n this article, we will address the con-cept of risk and the allegation that pes-ticide exposure is responsible for anincrease in cancer incidence. Readersare encouraged to review Part One,

which appeared in the June 2002 issue,for background information prior to read-ing this article. Part Three, which will ap-pear in the next issue, will address thesubjects of pesticide exposure and asthma,neurological affects in children, and en-docrine disruption. Please note that refer-ences for the complete three part seriesare footnoted in the text and a detailed list-ing is available from the Sports Turf As-sociation.

The Concept of Risk/HazardUnfortunately, a large portion of the

problem we are facing today with criesfrom the general public for a ban on theuse of pesticides for urban uses is relatedto misconceptions about risk. All activi-ties in which we participate carry a cer-tain element of risk. However, the public'sperception of risk is distorted because peo-ple haven't been taught about risk. Riskperception has more to do with a combi-nation of the frequency with which the riskis taken (familiarity with the activity), thelevel of control a person has over the riskysituation, how much pleasure they derivefrom it, and an unconscious decision toaccept certain risks because the benefitincurred outweighs the risk, than it does

the magnitude of the risk. For example,many people feel perfectly safe driving acar but unsafe when flying; when in real-ity, the risk of being seriously or fatallyinjured in a car accident is far greater thanbeing injured or dying in a plane crash.

Most of you reading this article prob-ably drink coffee, drive cars, ride bicyclesperiodically, and enjoy the occasional al-coholic beverage. Some of you are smok-ers. Many of you enjoy being out in thesun and don't always wear sunscreen, andmany have used a cell phone while driv-ing. The purpose of presenting this lengthylist of activities is to point out that peopletake risks everyday, whether they are driv-ing to work, crossing the street, riding abike, smoking a cigarette or consumingalcoholic beverages. Each of these activi-ties has a significant level of risk associ-ated with it, and each bears a much greaterhealth risk than you will ever incur fromexposure to pesticides used on turf. Un-fortunately, academia and the chemicalindustry have not effectively communi-cated the concept of risk to the generalpublic. Putting risk into perspective iscritical for the public to understand thatpesticides can be used safely with mini-mal risk to human health.

In 1982, Scientific American publisheda paper that ranked various activities ac-cording to their annual contribution to thenumber of deaths in the USl. A listing ofthe top ten, in order of the most hazard-

ous activities to the least hazardous, con-veys just how distorted the public's per-ception of risk truly is. The mosthazardous activity that a person can par-take in is smoking. More people die oftobacco-related illnesses than any othercause. The remaining top 10 in order are:use of alcoholic beverages, motor vehi-cles, handguns, electrical power, motor-cycles, swimming, surgery, x-rays andrailroads. Cycling ranked 13th, fire fight-ing and police work ranked 16th and 17threspectively, use of contraceptives 18th,vaccinations 25th, and "pesticides" ranked28th•

Certainly, each time a pesticide is han-dled there is some level of risk. "Risk" is

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a function of the inherent toxicity of a sub-stance and the exposure one has to it.

Risk = Toxicity x Exposure

Looking at this simple math equation,if the value for exposure is zero (no expo-sure), what happens to risk? It becomeszero. The most toxic substances known tohuman beings can be handled safely, withminimal risk, if there is little or no expo-sure. Alternatively, there can be consider-able risk involved in handling a compoundthat isn't very toxic if exposure is highenough. By keeping one, or both, of thesefactors as close to zero as possible, the riskinvolved in handling and using pesticidescan be minimized. Pesticide label direc-tions are designed to do just that.

Occupational and BystanderExposure

Scientists measure "exposure" and de-termine the amount of pesticide that isabsorbed into the body, because this rep-resents the internal dose. This internaldose is then compared to doses used inthe animal studies discussed in Part Oneof this article. There are three main routesof exposure into the body:

• Ingestion (oral exposure)• Contact (dermal exposure)• Inhalation (respiratory exposure,

what is breathed in)

Most occupational and bystander ex-posures to turf pesticides are a result ofexposure through the skin (dermal expo-sure) or lungs (respiratory exposure).

In 1992, Harris and Solomon investi-gated exposure to bystanders entering ar-eas where the turf had been treated withthe commonly used herbicide 2,4-D2• Ex-posure was measured by analyzing urinefor residues of 2,4-D. Exposures occur-ring 1 hour after herbicide applicationwere well below health protection guide-lines and 24 hours after spraying, nochemical exposures were measurable.Dislodgeable residues from the treated turffell from 8% to 1% during that period. The"rule of thumb" is that if treated surfacesare dry, exposure is reduced and is mini-mal. No detectable residues were found

12 AUTUMN 2002 I Sports Turf Manager

in the urine of 20 volunteers with the ex-ception of 3 people who were barefoot,wearing shorts and contacted turf withinone hour of application (which is againstlabel directions). No detectable residueswere found in the urine of volunteers ex-posed to treated tuif24 hours after appli-cation. At recommended application rates,exposure to turf sprayed with 2,4-D shouldpresent little risk to humans. Childrenshould never contact treated turf until it isdry, and should never be in the vicinityduring application.

A second study by the same lead au-thors examined exposure of homeownersmaking their own applications of 2,4-D,and exposure of household bystanders'.Residues were not detected in the urineof the bystanders. The only homeownerapplicators that had 2,4- D in their urinewere those who failed to wear protectivegear and had experienced spills of the liq-uid concentrate or had excessive contactwith the diluted mixture (residues rangedfrom non-detectable to 0.0071 mg/kgbodyweight, which is very low).

In 2001, Stephenson et al. measuredhomeowner applicator and bystander ex-po sure to liquid and granular (plus ferti-Iizer ) formulations of chlorpyrifos(Dursban) applied to turf". Urine was col-lected over a 96 hour period beginningimmediately after application. Of 40 by-stander study participants, only 4 had tracelevels of chemical metabolites detected intheir urine and only 1 had residues abovethe lowest quantifiable concentration (25ug/L). (Note: The term "trace" means themetabolite was detected but the quantitywas so low that an accurate measurementcould not be obtained.) This was expectedgiven the chemical properties ofchlorpyrifos and the fact that only 1.5 to3% of the chlropyrifos applied isdislodgeable immediately after applica-tion and less than 0.1 % is dislodgeable 1day after application'>.

Only 1 of 10 applicators who wore per-sonal protective equipment (PPE) hadtrace levels of metabolites in his urine fol-lowing application of the granular formu-lation, while 3 of 10 applicators who didnot wear PPE had detectable residues intheir urine (l trace and 2 quantifiable). Of11 volunteers wearing PPE and applying

the liquid formulation, 2 had traceresidues and 3 had quantifiable residuesin their urine. Certainly the use of protec-tive clothing reduced the extent of expo-sure. (Note: Dursban is no longerregistered for domestic home and gardenuses, the reasons for which are beyond thescope of this article; however, commer-cial formulations are available for use ongolf courses, industrial sites, sod farms,ornamental plantings and highway medi-ans.)

Many people are concerned about theirpets contacting treated turf. In 1991, awidely publicized study suggested a rela-tionship between canine malignant lym-phoma (CML) and exposure to 2,4-D7,8.

The study was highly criticized by expertsfor its design, as well as its analysis andinterpretation of the data. Unfortunately,once incorrect information is released tothe media, it is very difficult to refute orcorrect. The study data was reanalyzed byresearchers at Michigan State VeterinaryCollege who demonstrated that the datadid not confirm a dose-response relation-ship between 2,4-D use and CML, or evena significant association between the two".Studies are not available for all pesticidesused on turf; therefore, owners shouldkeep their pets indoors during pesticideapplication and until the turf is dry. Ascan be seen from the studies discussed,very little pesticide is dislodged fromtreated turf, particularly 24 hours afterapplication.

Pesticides and CancerThere has been a growing concern that

exposure to pesticides, either through foodresidues or when applied to home interi-ors, turf and gardens, may be a majorcause of various types of cancer. Concernhas been fuelled by some epidemiologystudies of pesticide manufacturers, appli-cators and farmers who have had highexposures and that are suggestive of anassociation with certain types of cancerssuch as prostate cancer and Non-Hodg-kin's Lymphoma (NHL).

There are many studies suggesting pes-ticide exposure increases cancer risk inthese populations and many indicating noeffect. These studies have been plaguedby small sample sizes (small numbers of

study participants) which reduces the sta-tistical power of a study, and flaws inher-ent in using questionnaires to obtainexposure data rather than actual sampleanalysis because the studies are "retro-spective" in nature; in other words, studyparticipants who have already been diag-nosed with cancer are asked to recall whatthey were exposed to 15 to 20 years ear-lier. The reason that exposures 15 to 20years earlier are important is that there isa latency period between the time thecausal exposure occurs and developmentof the disease. For many cancers, the la-tency period is close to 20 years. Obtain-ing accurate responses on a questionnaireis extremely difficult, if not impossible.In addition, few epidemiology studieshave accounted for confounding expo-sures to other compounds, including medi-cations, diesel fuel, etc.

Prior to discussing the results of epide-miology studies on pesticide exposure andcancer, it is critical for the reader to un-derstand what causes cancer and to be-come familiar with cancer incidence rates.

Basically, cancer is caused by the failureof the body's immune system to repairmutations (damage or errors) in our DNAthat in turn cause processes in the body'scells to go awry. DNA is the molecule wehave in each of our cells that carries ourown unique genetic code and also is re-sponsible for cell division.

In a healthy individual, cells continu-ally die and are replaced. Every time a celldivides and reproduces itself, there is anopportunity for an error to be made whenthe DNA duplicates. Every day, our bod-ies repair millions of mutations, most ofwhich are naturally occurring. This is oneof the roles of our amazing immune sys-tem. As we age, our DNA repair mecha-nisms start to falter and mutations that canlead to the growth of a tumour go uncor-rected. Consequently, the annual numberof newly diagnosed cancer cases increasesas the population ages.

Cancer can also be caused as a resultof exposure to an external stimulus that isextremely toxic to cells. If many cells arekilled, the body increases the rate of cell

division of the remaining cells to try andcompensate for the loss. With an increasein the rate of cell division, comes an in-creased risk that an error will be madewhen duplicating the DNA. In the end, itall comes down to a failure of our immunesystem to repair damage to DNA, whetherthe mutations are caused by a chemical,UV radiation from the sun, exposure tocigarette smoke or cancer causing virusesetc.

If pesticide exposure is contributing toan increase in cancer, this should be re-flected in age-adjusted cancer incidencerates over time. The graphs and data pre-sented in this article are from "CanadianCancer Statistics 2001" produced by theCanadian Cancer Society, the NationalCancer Institute of Canada, StatisticsCanada, Provincial/Territorial CancerRegistries and Health Canada". You canreview this information and more atwww.cancer.ca. On entering the website,select Research and Statistics, then Sta-tistics, Canadian Cancer Statistics 2001report. (Note, the 2002 report was recently

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Graphs 1 and 2. New cases and age-standardizedincidence rates (ASIRIfor all cancers, 1972-2001,males and females separately.

Males,00 ASIR ( .'er 100,000)

600

New Cases (OOOs) iO

FemalesASIR (per 100,000)

700 r-------------------, 70

New Cases (OOOs)

Ie

soo

400

New Cases --ASIR

Graphs 5 and 6. Average annual percent change (AAPC)in age-standardized incidence (1989-19961 and mortality(1989-1996) rates for selected cancer sites, males andfemales separately.

to

ThyroidProstate

Non-Hodgkin's LymphomaColoredal

Hodgkin's DiseaseBladder

LungLarynx

OralStomach

ThyroidLung

Non-Hodgkin's LymphomaBreast

LeukemiaHodgkin's Disease

ColorectalBladder

CervixStomach

Incidence Mortality

added to the website; however, the sum-mary in this article pertains to the 2001report). More specific data was obtainedfrom Cancer Surveillance On-Line http://cythera.ic. gc .ca/ dsol/cancer/" (exceptwhere noted, see references provided).

Canadian demographics are changing.The Canadian population is increasing andso is the average age of the population.As a result, the overall number of newlydiagnosed cases is increasing becausethere are more people around to developcancer and because the disease is moreprevalent in older people.

In order to remove aging and popula-tion increases as confounding factors incancer statistics, all cancer data is stand-ardized for age and presented as thenumber of new cases (incidence), ordeaths (mortality), per 100,000 of thepopulation. This allows data to be com-pared from year to year without popula-tion increases and average age of thepopulation complicating the issue.Graphs 1 and 2 depict the effect of stand-ardizing for age on the incidence numbersper 100,000 of the population in males and

14 AUTUMN 2002 I Sports Turf Manager

in females, respectively. These graphs alsodemonstrate that the age standardized in-cidence rate (ASIR) for all cancers com-bined has been relatively flat over theyears.

While the data presented are from 1972to 1996, the data prior to 1984 are not en-tirely accurate due to changing diagnos-tic criteria and inconsistencies in cancerregistry reporting. Inclusion of these datagives the impression that cancer incidencewas increasing during this time, whichmay not be true. The data from 1984 to1996 are much more reliable. The datafrom 1997 to 2001 are estimated valuesas the actual numbers have not yet beenpublished.

If we look at the age standardized inci-dence rates of various types of cancersindividually (Graphs 3 and 4), we cansee that, for most cancers, the incidencehas been flat or decreasing since 1983. Theonly cancers for which increases appearto be occurring are thyroid (not shown ongraph), lung, NHL and breast cancer inwomen, and NHL, thyroid (not shown ongraph), and prostate cancer in men. (The

FemalesIncreaseDecrease

increase in melanoma among older menand women will not be specifically ad-dressed here as this is believed to be dueto UV exposure.) These trends are alsoapparent in the average annual percentchange in cancer incidence and mortality(1989 - 1996) for men and women

Graph 3. Age-standardized incidencerates (ASIRIfor selected cancer sites,males, 1972-2001.

151) ;.:.A~SI.:.;;.R..u;..;:.;:....;..::.=.:~,---- ......,

se ....- ....... /'-------, Bladder-::::::::"·-.~,~-v,,~?~~~~~~==:-=::'j~ ~~:H,2~j1~ipsJ.~mphomcr"'0-~" -~_0", _

Melanoma

(Graphs 5 and 6). One trend not appar-ent from these graphs is the increase inthe incidence of testicular cancer in menaged 20 - 49 years. Looking at these spe-cific cancers individually, several com-ments can be made. (Note: Lung cancerin women will not be specifically ad-dressed as it is widely acknowledged thattobacco use is responsible for the in-creased incidence of this disease.)

Graph 4. Age-standardized incidencerates (ASIR)for selected cancer sites,females, 1972-2001.

ASIR ( er 100,000)

Thyroid CancerThyroid cancer is more prevalent in

women than men. An increased incidenceof thyroid cancer between 1984 and 1998has indeed been observed in women 20 -49 years of age. The magnitude of thisincrease has not, however, been observedin males of similar age; the increase inmales has been small during the same timeperiod.

It is interesting to note that the inci-dence of this type of cancer took a jumpbetween 1991 and 1995 in both sexes andmost age groups suggesting improved de-tection of this type of lesion; however, thisdoes not explain the dramatic increaseamong women compared to men.

In the early 1990s, the increased use offine-needle aspiration biopsy may accountfor a portion of this increase. Incidenceof thyroid cancer rises slowly with age.Many studies have linked exposure to ra-diotherapy directed to the neck region dur-ing childhood with a significantly

increased risk of thyroid cancer. Externalexposure during adulthood and internalexposure to therapeutic or diagnosticdoses of radioactive iodine, however, donot appear to increase risk. Changes iniodine intake may increase the incidenceof some types of thyroid cancer and de-crease the incidence of others. Diet mayplaya role, with consumption of vegeta-bles (e.g. cruciferous) conveying somelevel of protection. Due to the differencein incidence between men and women,hormonal factors may be responsible.While studies have been conducted to as-sess a possible relationship between thy-roid and breast cancers, the associationsdemonstrated have been weak, study sam-ple sizes small and the conclusions notalways consistent.

Non-Hodgkin's lymphoma (NHL)The incidence of non-Hodgkin's lym-

phoma (NHL) has increased in both sexesof the 20 - 49 year old age group between1984 and 1998, with the incidence, as wellas the percentage increase, being greaterin males than females.

The risk of NHL increases with age.Patients treated with radiation therapy forother cancers are at increased risk of de-veloping NHL, and those treated with bothradiation and chemotherapy are at evengreater risk. Epstein-Barr virus has beenassociated with some uncommon types ofNHL. HIV is a risk factor for NHL andthe incidence among AIDs patients ismuch higher than in the general public;consequently, any increase in the inci-dence of HIV and AIDS will result in aconcomitant increase in the incidence ofNHL. Since the incidence of HIV andAIDS is rising more rapidly among menthan women, it would be expected that agreater increase in the incidence of NHLin men would be observed.

Several epidemiology studies have con-cluded associations between exposure tophenoxy herbicides such as 2,4-D andMCPA, which are commonly used in ag-riculture and on turf, and the developmentof NHL18,19,20,21.The majority of thesestudies have not measured exposure di-rectly and failed to account for concomi-tant exposures to potential carcinogens(e.g. diesel fuel, prescription drugs) and

exposure to oncogenic viruses found orsuspected to playa role. In some studies,associations were found with certain oc-cupations only; however, more researchis required on this subject because defini-tive conclusions cannot be drawn from theepidemiology studies currently available.

Breast CancerThe increased incidence of breast can-

cer in women may be due to lifetime ex-posure to estrogen which stimulates bothnormal and abnormal breast cell develop-ment". Lifestyle changes such as havingfewer children, giving birth at a later ageand a reduction in the duration of breast-feeding or not breast-feeding at all, in-crease lifetime exposure to endogenousestrogen. High fat diets and genetics(BRCAI and BRCA2 genes) also playarole. The use of oral contraceptives andhormone replacement therapy have beenimplicated as causal factors; the formerby allowing women to delay pregnancyuntil a later age and the extent of the latterbeing dependent on the duration of treat-ment in addition to other factors. A por-tion, but not all, of the increase inincidence can be attributed to improveddiagnostic techniques (the increased useof mammography).

Apparent from Graph 4, is that the in-crease in the incidence of breast cancerseems to be paralleling an increase in theincidence of lung cancer in women sug-gesting an association between the twodiseases. While the incidence of lung can-cer in males has declined due to a reduc-tion in smoking among men, the incidenceof lung cancer in women is still on the rise.The number of smokers in the femalepopulation has not declined to the sameextent as among males, which would ex-plain this statistic.

Prostate CancerThe incidence of prostate cancer among

men rose very slowly from 1984 to 1988.The dramatic increase in the incidence ofthis cancer between 1989 and 1993 canbe explained by improved diagnostic tech-niques - primarily the use of Prostate Spe-cific Antigen (PSA) testing. The increasein incidence occurred just after this newtechnique was introduced.

www.sportsturfassociation.comIAUTUMN 2002 lS

There has been a subsequent decline inincidence since 1993, as existing caseswere diagnosed. This is truly indicativeof an increase due to improved diagnos-tics. Risk factors include a family historyof prostate cancer, high fat diet and vita-min D deficiency. Findings in epidemiol-ogy studies of occupation and prostatecancer risk have suggested a slightly in-creased risk among farmers, athletes,power plant workers, firefighters, work-ers in leather processing industries andsoap/perfume manufacturing; however,the casual risk factors have not been con-firmed''" 24, 25.

Testicular CancerThe incidence of testicular cancer has

increased steadily in men aged 20 - 49from approximately 6 cases per 100,000of the population in 1984 to 8.5 cases in1998. Incidence among men aged 50 andover has been flat to slightly declining (ac-tual number of cases is low at appro xi-mately 1 - 2 per 100,000 each year).

The main risk factors for testicular can-cer are cryptorchidism or undescendedtesticle( s) and a family history of the dis-ease, suggesting a genetic component.Approximately 14% of the diagnosedcases occur in men with cryptorchidism.There is an increased incidence amongmen with white collar or professional oc-cupations as opposed to those who wouldbe involved in manufacturing or sprayingpesticides. This observation suggests so-cioeconomic status or lifestyle may be as-sociated with the disease. It does notsuggest that pesticide exposure is respon-sible. Exposure to "endocrine-disruptingchemicals" has been suggested as a pos-sible contributing factor; however, it hasnot yet been demonstrated that the levelof exposure the average public incurs tosuch chemicals originating from a varietyof sources, including those that are natu-ral, is sufficient to cause such a response.

Childhood CancersThere has been a great deal of public-

ity suggesting that the incidence of child-hood leukemia is increasing and thatpesticides are responsible. Actually, theincidence of leukemia in children is notincreasing in Canada or in the US. Inci-

16 AUTUMN 2002 I Sports Turf Manager

dence of leukemia inCanadian boys has re-mained relatively flataround a mean of 4.6cases per 100,000 dur-ing the period from1984 to 1998. Incidencehas also been relativelystable among girls (ap-proximately 3.9 casesper 100,000) during thesame period. The inci-dence of leukemiapeaks in children 1 to 4years of age at appro xi-mately 8 cases per100,000 and declinesafterwards to approxi-mately 2.5 cases per100,000 in children 10to 14 years of age.

Epidemiology stud-ies suggesting an asso-ciation betweenpesticide exposure andchildhood leukemia areflawed due to smallsample sizes and lack ofstatistical power, recallbias (asking a mother after her child hasbeen diagnosed with cancer to rememberwhat she was exposed to during her preg-nancy and what her baby was exposed toafter birth), failure to quantitatively meas-ure exposure to pesticides and the iden-tity of those pesticides, estimatingexposure from birth certificate data orparental occupational title instead of ac-tual sample measurements, and failure tocontrol for confounding factors such asother exposures, just to name a few.

In 1998, Hoar Zahm and Ward of theUS National Cancer Institute published areview paper summarizing data in the lit-erature on pesticide exposure and cancerrisk in children". Their paper states that,while the studies reviewed were limitedby a lack of pesticide exposure informa-tion, small sample sizes and the risk ofrecall bias (plagued by memory and othercomplicating factors), the risks reportedwere greater than those reported for pes-ticide exposed adults suggesting that chil-dren may be more sensitive to thecarcinogenic effects of pesticides. (Note:

More research is required; however, in the meantime, we shouldreduce the exposure of children to pesticides, not reduce theuse of pesticides. The leading cause of death among Canadianchildren is not cancer - it's injuries.

The results could also indicate that par-ents more readily implicate pesticideswhen questioned about their child's ex-posure, compared to their response regard-ing their own exposure.)

The authors concluded that future re-search must include better methods forquantifying exposure to pesticides, inves-tigation ofthe possibility of genetic-envi-ronmental interactions, etc. These arereasonable suggestions. The authors alsoconcluded that reducing or eliminatingpesticide exposure has the potential to pre-vent at least some childhood cancers. Thisis one conclusion that many scientists be-lieve is a "leap" considering the weak-nesses of the studies cited.

A year later, 5 researchers from thesame institution published a review paperthat concluded that increases in childhoodcancer can be explained by improved di-agnostic techniques", Linet et al. exam-ined incidence and mortality patternsamong 14,540 children under the age of15 years that were diagnosed with cancerfrom 1975 to 1995. They concluded that

there was no substantial change in inci-dence for the major pediatric cancers andrates have remained relatively stable sincethe mid-1980s. The modest increases thatwere observed for brain/central nervoussystem (CNS) cancers, leukemia and in-fant neuroblastoma, were confined to themid-1980s. This pattern suggests that in-creases likely reflect diagnostic improve-ments or reporting changes that occurredduring that time.

The subject of pesticide exposure andchildren's cancer risk is an emotional oneand determining whether or not a relation-ship exists is quite complicated". Evenresearchers from the US National CancerInstitute have differing opinions on thesubject; however, those who believe thatthere is a connection concede that expo-sure has not been well defined and thatthe available studies investigating pesti-cide use and the development of pediatriccancers have many additional flaws in-cluding small sample sizes and case-con-trol bias.

More research is required; however, inthe meantime we should reduce the expo-sure of children to pesticides, not reducethe use of pesticides. As was seen fromthe Harris and Solomon (1992), andStephenson et al. (2001) data, applying thecorrect application rate of a turf pesticide,and restricting contact with treated turf fora 24 hour period will result in non-detect-able residues among bystanders, whichtranslates to no detectable exposure to in-dividuals contacting treated turf'".

(Note: The leading cause of deathamong Canadian children is not cancer -it is injuries". Many ofthese "accidental"deaths are preventable. Injury mortalitystatistics include deaths due to uninten-

tional injuries such as motor vehicle acci-dents and falls, in addition to deaths dueto suicide and assault (including childabuse). In 1996, 16 deaths per 100,000occurred in people under age 20 due toinjuries. This is equivalent to 30.5% of alldeaths in this age group.)

Conclusions of Scientific ReviewPanels and Authors of ReviewPapers on the Subject ofPesticides and Cancer

In 1997, the National Cancer Instituteof Canada's Advisory Committee on Can-cer Control (ACOCC) addressed the is-sue of public exposure to pest controlproducts to determine whether a signifi-cant level of risk existed that would ne-cessitate the Canadian Cancer Societychanging its priorities which are currentlyfocused on tobacco control strategies.ACOCC established an Ad Hoc panel onpesticides and cancer". While the Ad Hocpanel concerned itself primarily with pes-ticides used in the agricultural scenario,the published conclusions of this panelwere that: no association was found be-tween pesticide use and cancer and sev-eral factors may reduce cancer ratesincluding:

• Reduction in smoking• Increased consumption of fruits and

vegetables• Control of infections• Avoiding intense exposure to sunlight• Increasing physical activity• Reducing alcohol consumption

The following year, world-renownedepidemiologist, Sir Richard Doll reviewedthe published literature on potential causes

Table 1. HERP Percentage Values for Common Substances

Beer (257 g) Ethyl alcohol 2.8

0.1Coffee (13.3 g) Caffieic acid

Bacon (100 g) 0.003Diethylnitrosamine

Lindane, daily dietary intake Lindane 0.000001

0.00000001Chlorothalonil (Daconil),daily dietary intake

Chlorothalonil

of cancer and drew conclusions very simi-lar to those of the Ad Hoc panel", He con-cluded that smoking, alcohol,pharmaceutical products, infection, elec-tromagnetic radiation (ionizing, UV, lowerfrequency), occupation, industrial prod-ucts, pollution (air, water, food), physicalinactivity, reproductive hormones and di-etary factors (not pesticide related) wereall causes of cancer.

Smoking and dietary factors are themost important, responsible for approxi-mately 30%, and 20 to 50% of fatal can-cers, respectively. Occupation, industrialproducts and pollution (including pesti-cides) combined, were thought to be re-sponsible for a total of 3 to 4% of all fatalcancers.

In addition to other benefits, increased con-sumption of fruits end vegetables mayreduce cancer rates.

Doll stated that there is no sound, sci-entific evidence to suggest that pollutionfrom all sources, including pesticides, isa significant cause of cancer. The 9th Re-port on Carcinogens, published in 2000by the US Dept. of Health and HumanServices/National Toxicology Program,listed over 50 compounds known to behuman carcinogens". Not one pesticidewas included on this list. The criteria usedto define "known" were that "there is suf-ficient evidence of carcinogenicity fromstudies in humans which indicates a causalrelationship between exposure to theagent, substance or mixture and humancancer .... "

www.sportsturfassociation.comIAUTUMN 2002 17

On the list are items such as aflatoxinsproduced by a fungus that grows on nuts,alcohol, asbestos, arsenic, coal tar,diethylstilbesterol (DES), tobacco smok-ing, environmental tobacco smoke,smokeless tobacco, exposure to UV lightfrom solar radiation, sun lamps and tan-ning booths, crystalline silica andtamoxifen. Tamoxifen is a drug used verysuccessfully to combat breast cancers thatgrow in response to estrogen. Tamoxifenalso increases the risk of endometrial can-cer, a form of uterine cancer, which is whyit is listed; however, the risk of develop-ing endometrial cancer is so small in com-parison to the benefit gained amongwomen with breast cancer that the drug iswidely used and will not be banned.Things come full circle to risk versus ben-efit. The major causes of cancer listed inthe "9th Report" were:

• Smoking• Dietary imbalances (insufficiency of

many micronutrients, insufficientconsumption of fruits and vegetables)

• Hormonal factors, primarilyinfluenced by lifestyle

• Chronic infections, mostly indeveloping nations

• Inflammation• Genetic factors

In 1987, Ames et al. developed a rank-ing of carcinogenic substances to provideinsight into the real risks that threaten ourquality and length of life33. Often the threatto our health is not from rigorously testedproducts like pesticides, but from othersubstances to which we have uncon-sciously accepted the risks involved forthe benefits obtained.

Table 1 (on the previous page) lists afew of the substances Dr. Ames has rankedusing his Human ExposurelRodent Po-tency (HERP) Index.

We test carcinogens on animals nothumans and measurements are expressedas the rodent carcinogenic potency. Torelate a product's carcinogenic potentialin rodents to its carcinogenic potential inhumans, the Rodent Carcinogenic Potency

values are converted to HERP values. Thehigher the HERP % the greater the carci-nogenic risk to humans. As you can see,the carcinogenic potential of beer and cof-fee are far greater than that of Lindane,an organochlorine insecticide orchlorothalonil, a fungicide that is com-monly used on turf.

ConclusionsReviews of sound, scientific, peer-re-

viewed data, indicate that allegations sug-gesting occupational and bystanderexposure to pesticides is associated withincreased cancer incidence, is currentlyunfounded. Unfortunately, the media'spresentation of possible associations hascreated an irrational fear about pesticidesamong the general public.

As mentioned in Part One of this arti-cle' any pesticide ban approved by a mu-nicipality is a political decision based onemotion and not one based on sound sci-ence. This fact should be clearly commu-nicated to the constituents of themunicipalities involved. •

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