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Human health effects of agrichemical use.Hum
Pathol. 1993 Jun;24(6):571-6.
The use
of pesticides and nitrogen fertilizers in agriculture has grown
dramatically over the past 30 years. Currently, approximately 600
active pesticide ingredients are used, but adequate toxicologic data
are available for only approximately 100 of these. Environmental
exposure of humans to agrichemicals is common and results in both
acute and chronic health effects, including acute and chronic
neurotoxicity (insecticides, fungicides, fumigants), lung damage (paraquat),
chemical burns (anhydrous ammonia), and infant methemoglobinemia
(nitrate in groundwater). A variety of cancers also have been linked
to exposure to various pesticides, particularly hematopoietic
cancers. Immunologic abnormalities and adverse reproductive and
developmental effects due to pesticides also have been reported. The
health effects associated with pesticides do not appear to be
restricted to only a few chemical classes. Therefore, enhanced
efforts are needed to control or eliminate human exposures wherever
possible. Research also is needed to better characterize and
quantitate the adverse effects of agrichemicals on human health.
Agricultural chemical utilization and human health.
Environ Health Perspect. 1992 Jul;97:269-74.
The public is
justifiably concerned about the human health effects of agricultural
chemicals. The many gaps in information about the mechanisms of
toxic action, human exposures, and the nature and extent of human
health effects are large. Very few older pesticides, in particular,
have been tested for human health effects. Workers who produce,
harvest, store, transport, process, and prepare food and fibers are
exposed to many chemicals that are potentially hazardous and that
are used in agriculture. The occupational health of these workers
has not been adequately studied, and protective efforts have
sometimes been minimal. Valid and accurate risk assessment is best
based on sound information about how chemicals, in this case
agricultural chemicals, are involved in toxic events--their
mechanisms of action. These health effects include tumor promotion,
chronic and acute neurotoxicity, immunotoxicity, and reproductive
and developmental toxicity. Another key part of risk assessment is
exposure assessment. Fundamental studies of the toxicology of target
organisms and nontarget organisms exposed to agricultural chemicals
are needed to discover and develop better solutions to the problems
of agricultural pest control, including better formulations, optimal
application rates and public education in safety and alternative
agricultural practices. The large number of pesticides that have
never been adequately tested for effects on human health is
particularly worrisome in light of emerging information about
delayed nervous system effects.
Biological Monitoring of Pesticide Exposure: a
review. Introduction.Toxicology.
2000 Feb 7;143(1):1-118.
Pesticides are
used worldwide in agriculture, industry, public health and for
domestic applications: as a consequence, a great part of the
population may be exposed to these compounds. In spite of this
extensive use, knowledge on the health risks associated with
prolonged exposure is rather poor, and major uncertainties still
exist. Epidemiological observations in man have so far produced
little conclusive information, mainly because of weaknesses in
exposure assessment. Therefore, information on the type and levels
of exposure is fundamental in order to better understand and
characterize risk to human health. Exposure assessment can be
carried out via measurement of environmental concentrations, as well
as via determination of the chemical or its metabolites in body
tissues (biological monitoring). Besides indices of internal dose,
biological monitoring also includes measurements of early effects
attributable to interaction between the chemical agent and the human
body. Biological monitoring has the advantage, over environmental
monitoring, of determining the dose actually absorbed via any
possible route: differences in absorption can be taken into account.
whether they are due to biological variability or to use of
protective equipment. When, in some cases, a combination of
occupational and non-occupational exposure occurs, this also can be
taken into consideration by biological monitoring. Few reference
documents have been published on biological monitoring of
pesticides. For this reason, the Office of Occupational Health of
the World Health Organization gave ICPS a mandate to prepare a
monograph specifically addressed to reviewing methods for biological
monitoring of pesticide exposure. This review is based on more than
300 studies published over the period 1980-1999. For the most
representative chemical classes, the available biological exposure
indices are reported. Both indices of internal dose and. when
available, of early effects are discussed. The reported tests were
used to monitor exposure of pesticide applicators in agriculture and
public health, manufacturing and formulating workers. subjects
poisoned after accidental exposure or attempted suicide, volunteers
involved in pharmacokinetic studies, as well as sub-groups of the
general population exposed to environmentally persistent pesticides.
Single chapters deal with organophosphorus insecticides, carbamate
pesticides, dithiocarbamates, phenoxyacids, quaternary ammonium
compounds. coumarin rodenticides, synthetic pyrethroids,
organochlorine pesticides, chlorotriazines, and pentachlorophenol.
Parkinson's disease in diphenyl-exposed workers--a
causal association?Parkinsonism
Relat Disord. 2006 Jan;12(1):29-34.
Epub 2005 Oct 26.
We report a
cluster of five cases of Parkinson's disease (PD) among paper mill
workers exposed to a fungicide, diphenyl. The cause of PD is still
unknown, but epidemiological studies have indicated an elevated risk
of developing PD after exposure to pesticides. The five cases of PD
were found in a group of 255 diphenyl-exposed workers, and the
number of expected cases in the exposed group was estimated to be
0.9, resulting in a relative risk of 5.6 (95% CI 1.8-13). Exposure
to diphenyl may have contributed to this PD cluster, but chance is
an alternative explanation.
The
epidemiology of pesticide exposure and cancer: A review.Rev
Environ Health. 2005
Jan-Mar;20(1):15-38.
Cancer is a
multifactorial disease with contributions from genetic,
environmental, and lifestyle factors. Pesticide exposure is
recognized as an important environmental risk factor associated with
cancer development. The epidemiology of pesticide exposure and
cancer in humans has been studied globally in various settings.
Insecticides, herbicides, and fungicides are associated with
hemopoetic cancers, and cancers of the prostate, pancreas, liver,
and other body systems. The involvement of pesticides in breast
cancer has not yet been determined. In developing countries,
sufficient epidemiologic research and evidence is lacking to link
pesticide exposure with cancer development. Agricultural and
industrial workers are high-risk groups for developing cancer
following pesticide exposure. Children of farm workers can be
exposed to pesticides through their parents. Maternal exposure to
pesticides can pose a health risk to the fetus and the newborn. The
organophosphates are most the commonly used compounds, but the
organochlorines are still permitted for limited use in developing
countries. Pesticide exposure, independently or in synergism with
modifiable risk factors, is associated with several types of cancer.
Association of pesticide exposure with neurologic dysfunction and
disease.Environ
Health Perspect. 2004 Jun;112(9):950-8.
Poisoning by
acute high-level exposure to certain pesticides has well-known
neurotoxic effects, but whether chronic exposure to moderate levels
of pesticides is also neurotoxic is more controversial. Most studies
of moderate pesticide exposure have found increased prevalence of
neurologic symptoms and changes in neurobehavioral performance,
reflecting cognitive and psychomotor dysfunction. There is less
evidence that moderate exposure is related to deficits in sensory or
motor function or peripheral nerve conduction, but fewer studies
have considered these outcomes. It is possible that the most
sensitive manifestation of pesticide neurotoxicity is a general
malaise lacking in specificity and related to mild cognitive
dysfunction, similar to that described for Gulf War syndrome. Most
studies have focused on organophosphate insecticides, but some found
neurotoxic effects from other pesticides, including fungicides,
fumigants, and organochlorine and carbamate insecticides. Pesticide
exposure may also be associated with increased risk of Parkinson
disease; several classes of pesticides, including insecticides,
herbicides, and fungicides, have been implicated. Studies of other
neurodegenerative diseases are limited and inconclusive. Future
studies will need to improve assessment of pesticide exposure in
individuals and consider the role of genetic susceptibility. More
studies of pesticides other than organophosphates are needed. Major
unresolved issues include the relative importance of acute and
chronic exposure, the effect of moderate exposure in the absence of
poisoning, and the relationship of pesticide-related neurotoxicity
to neurodegenerative disease.
Pesticide poisoning.
An Sist Sanit Navar. 2003;26 Suppl
1:155-71.
Pesticides
are one of the families of chemical products most widely used by
man. They have been used above all to combat pests because of their
effect on harvests and as vectors of transmissible diseases.
Pesticides can be classified according to their use (insecticides,
fungicides, herbicides, raticides em leader ) or by their chemical
family (organochlorates, organophosphates, carbamates, pyrethroids,
Bipyridilium compounds, inorganic salts em leader ). All of them are
biocides, which normally implies a high toxicity for humans, which
has been a cause for concern since the mid-XX century due to the
widespread and indiscriminate use of these products. Exposure to
pesticides can have effects that are acute, chronic and long-term.
Some organochlorate compounds (such as DDT) were the first to be
used in massive fumigations to fight malaria and have had to be
banned because of their capacity for bioaccumulation and
environmental persistence. The danger represented by the widespread
presence of these agents has been demonstrated in numerous episodes
of human toxic epidemics, producers of a high morbidity/mortality,
described for nearly all chemical families: organochlorate
insecticides and fungicides, organophosphate and carbamate
insecticides, organomercurial fungicides and inorganic salts. These
episodes have above all been caused through the ingestion of
foodstuffs and in the occupational field. Other causes of health
concern are their carcinogenic capacity and occasional reproductive
alterations. The principal characteristics of some of the most
relevant families are presented.
Developmental exposure to the pesticides paraquat and maneb and the
Parkinson's disease phenotype.
Neurotoxicology. 2002
Oct;23(4-5):621-33.
Idiopathic
Parkinson's disease (PD) is associated with advanced age, but it is
still unclear whether dopaminergic neuronal death results from
events initiated during development, adulthood, or represents a
cumulative effect across the span of life. This study hypothesized
that paraquat (PQ) and maneb (MB) exposure during critical periods
of development could permanently change the nigrostriatal dopamine
(DA) system and enhance its vulnerability to subsequent
neurotoxicant challenges. C57BL/6 mice were treated daily with
saline, 0.3 mg/kg PQ, 1 mg/kg MB or PQ + MB from post-natal (PN)
days 5 to 19. At 6 weeks, a 20% decrease in activity was evident
only in the PQ + MB group, with a further decline (40%) observed at
6 months. A subset of mice were re-challenged as adults with saline,
10 mg/kg PQ, 30 mg/kg MB, or PQ + MB 2 x a week for 3 weeks. Mice
exposed developmentally to PQ + MB and rechallenged as adults were
the most affected, showing a 70% reduction in motor activity 2 weeks
following the last rechallenge dose. Striatal DA levels were reduced
by 37% following developmental exposure to PQ + MB only,
butfollowing adult re-challenge levels were reduced by 62%. A
similar pattern of nigral dopaminergic cell loss was observed, with
the PQ + MB treated group exhibiting the greatest reduction, with
this loss being amplified by adult re-challenge. Developmental
exposure to PQ or MB alone produced minimal changes. However,
following adult re-challenge, significant decreases in DA and nigral
cell counts were observed, suggesting that exposure to either
neurotoxicant alone produced a state of silent toxicity that was
unmasked following adult re-exposure. Taken together, these findings
indicate that exposure to pesticides during the PN period can
produce permanent and progressive lesions of the nigrostriatal DA
system, and enhanced adult susceptibility to these pesticides,
suggesting that developmental exposure to neurotoxicants may be
involved in the induction of neurodegenerative disorders and/or
alter the normal aging process.
Familial
nasal NK/T-cell lymphoma and pesticide use.
Am J Hematol. 2001;66(2):145-7.
Familial occurrence of nasal NK/T-cell lymphoma (NNKTCL) in
pesticide users is presented. The proband (71 years old, male) and
son (39 years old) were both diagnosed with NNKTCL within interval
of 26 months. Laboratory data showed slight anemia, with no abnormal
cells in peripheral blood. They and their wives were farmers and
used large amounts of pesticides (fungicides and insecticides) in
the hothouse. NNKTCL did not develop in the wives. Proband's father
was diagnosed with malignant lymphoma of the neck and died of the
disease. Genetic analyses of the peripheral blood leukocytes and
tumor tissues did not show p53 and k-ras gene mutations and
microsatellite instability. Metaphase cells from peripheral blood
leukocytes bore specific marker chromosomes (father,
44XY,-14,-17,-18,-22,+2mar; son, 46XY,-17,+1mar). Environmental
exposures to pesticides in conjunction with familial or genetic
factors might increase the risk for NNKTCL.
Environmental exposure to hexachlorobenzene (HCB) and risk of female
breast cancer in Connecticut.Cancer
Epidemiol Biomarkers Prev. 1999
May;8(5):407-11.
Earlier
studies have provided inconclusive results relating
hexachlorobenzene (HCB), an organochlorine fungicide, to female
breast cancer risk. The current study, with a total of 304 breast
cancer cases and 186 controls recruited in Connecticut between 1994
and 1997, examined the association by directly comparing breast
adipose tissue levels of HCB between incident breast cancer cases
and noncancer controls. The cases and controls were patients who had
breast biopsies or surgery at the Yale-New Haven Hospital (New
Haven, CT) and histologically diagnosed either as breast cancer or
benign breast disease. Information on major known or suspected risk
factors for breast cancer was obtained through in-person interview
by trained interviewers. No significant difference in mean breast
adipose tissue levels of HCB was observed between breast cancer
patients (21.0 ppb) and controls (19.1 ppb) in this large
case-control study. The risk also did not vary significantly by
menopausal status, estrogen or progesterone receptor status of the
breast cancer cases, breast cancer histology, stage of diagnosis, or
type of benign breast disease. Among parous women who reported ever
breast feeding, an odds ratio (OR) of 0.5 [95% confidence interval
(CI), 0.2-1.4] was observed when the highest quartile was compared
with the lowest quartile. However, no association was observed among
parous women who reported never breast feeding (OR = 0.7; 95% CI,
0.3-1.7 for the fourth quartile). For nulliparous women, the
adjusted OR was 2.1 (95% CI, 0.5-8.8) for the third tertile when
compared with the lowest based on few subjects. Therefore, our study
does not support a positive association between environmental
exposure to HCB and risk of breast cancer.
Chlororganic pesticides and polychlorinated biphenyls in breast
tissue of women with benign and malignant breast disease.Arch
Environ Contam Toxicol. 1998
Jul;35(1):140-7.
Persistent
chlorinated hydrocarbons assimilated through the diet may, as a
result of their carcinogenic, immunotoxic, and, at least in regard
to certain of these substances, estrogenic properties, play a role
in the etiology of human breast cancer. As a consequence, increased
concentrations of these ubiquitous environmental contaminants may be
found in breast tissue of women suffering from malignant breast
disease. To examine this possibility, surgically removed breast
tissue samples from 65 women in Hesse, Germany were examined by
capillary gas chromatography for p, p'-dichloro(diphenyl)trichloroethane
(p,p'-DDT), p, p'-dichloro(diphenyl)-dichloroethane (p,p'-DDD), p,
p'-dichloro(diphenyl)dichloroethene (p,p'-DDE), hexachlorobenzine (HCB),
alpha-, beta-, and gamma-hexachlorocyclohexane (HCH) as well as the
polychlorinated biphenyls (PCB) no. 28, 31, 49, 52, 101, 105, 118,
138, 153, 156, 170, and 180. Of the 65 patients, 45 were diagnosed
with breast cancer. The control group of 20 women suffered from
benign breast disease such as mastopathy. After statistical
adjustment for age differences, higher concentrations of p,p'-DDT,
p, p'-DDE, HCB as well as PCB-congeners no. 118, 138, 153, and 180
were detected in tissue from women with breast cancer than in tissue
from control persons. These differences were weakly significant for
p, p'-DDE (p = 0.017), for PCB 118 (p = 0.042) and for PCB no. 153
barely not significant (p = 0.083). On an average, a 62% higher
concentration of p,p'-DDE was found in cancer tissue (cancer
patients: 805 microg/kg fat; controls: 496 microg/kg fat) and 25%
higher concentration of PCB no. 118 (81 microg/kg fat; 65 microg/kg
fat). The concentrations of beta-HCH, PCB no. 156 and 170 were lower
(not significant) in cancer tissue than in tissue from women with
benign disease. PCB-congeners no. 105 and 149 as well as gamma-HCH
could only be detected in individual tissue samples; congeners no.
28, 31, 49, 52, and 101 as well as alpha-HCH and p,p'-DDD were not
detected in any of the samples. To rule out the possibility that the
concentrations of chlorinated hydrocarbons measured were influenced
by the surgical procedure, 20 samples of tissue that were at a
distance (minimum 1 cm and maximum 3 cm) from the tumor, tissue that
was in direct proximity to the tumor (no more than 5 mm from the
tumor), and tumor tissue itself (center of tumor) were separately
prepared and analyzed. The average concentrations of chlorinated
hydrocarbons varied to differing degrees and only minimally in tumor
and surrounding breast tissue, indicating that the surgical
procedure did not influence the results.
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