Public Health Significance of Urban Pests
487
an acute hazard in normal use no category. Most of the recently registered compounds are classified as presenting slight or no acute hazard. For our discussion on pesticide
hazards in residential settings, Fig. 14.2 shows the oral LD
50
values for rats for some of the most commonly used household biocides.
14.3.1.1.1. Epidemiology of acute pesticide poisoning Our knowledge of the effects of pesticides on people generally comes from reports of
acute poisoning that occur worldwide. Acute pesticide poisoning can result from inten- tional, occupational or accidental exposure to pesticides, but worldwide figures of pesti-
cide poisonings are not available. WHO the United Nations Environment Programme WHO, 1990 estimated an annual incidence of unintentional acute poisoning of about 1
million people, with an overall mortality rate of about 1 of which only 1 is in middle- and high-income countries. The majority of unintentional pesticide poisonings are occu-
pational, although cases occur in the general population due to improper use or storage of pesticides intended for amateur uses or in-house pest control. The most hazardous
compounds cause the majority of these poisonings. Population-based studies in 17 coun- tries gave annual incidence rates of unintentional pesticide poisoning of 0.3–18.0 cases
per 100 000 population Jeyaratnam, 1990.
Pesticides are estimated to be responsible for less than 4 of deaths from all types of acci- dental poisoning, based on reports from poison control centres: the apparent increase in
the number of cases in recent years may reflect increased use, but it may also reflect the availability of better statistics. The estimated annual incidence of intentional acute poi-
soning is about 2 million people, with a 5.7 mortality rate, which appears to be higher in low-income countries up to 23 WHO, 1990. Suicide attempts usually, but not
exclusively, with organophosphorous compounds represent 44–91 and 26–60 of acute pesticide poisonings in South-East Asia and in Central America, respectively, whereas in
California all non-occupational pesticide poisonings represent about 5 of the total Jeyaratnam, 1990. An unknown fraction of these attempts involves pesticides intended
for uses other than agriculture. WHO Peden, McGee Krug, 2002 reports accidental pesticide poisonings as the ninth leading cause of death.
14.3.1.2. Toxicity end-points
Standardized sets of toxicological tests are used to screen a pesticide for toxicity, and the results are used to construct the pesticide’s toxicology profile. Ultimately, this results in
the identification of the dose–response relationship for toxic end-points of concern to human health. A dose level that causes no observed adverse effect NOAEL is generally
used to identify safe levels of intake reference dose, which are then compared with the expected or measured exposure. Generally, the reference dose acute, short-term, or long-
term is derived from the NOAEL for the most relevant effect, by applying to its value, a factor called safety or uncertainty factor to take into account such issues as species
extrapolation, individual variability and quality of the toxicological database. T he NOAEL values selected for the reference dose vary according to the exposure scenario
that needs to be assessed.
Pesticides: risks and hazards
486
is based primarily on acute oral and dermal toxicity lethal dose, 50 [LD
50
] to rats used in experiments, since these determinations are standard procedures in toxicology. The
LD
50
value is a statistical estimate of the number of milligrams of toxicant per kilogram of body weight required to kill 50 of test animals. Provision is made for adjusting the
classification of a particular compound if, for any reason, the acute hazard to people dif- fers from that indicated by LD
50
assessments alone. Among other considerations, classi- fication adjustments are made for the following reasons.
• If it is shown that the rat is not the most suitable test animal, then data from species other than the rat are used.
• If the AI produces irreversible damage to vital organs, is highly volatile, is markedly cumulative in its effect, or is found after direct observations to be particularly hazar-
dous or significantly allergenic to human beings, then it can be classified
in a higher hazard category.
Table 14.1 shows the criteria used to clas- sify solid and liquid pesticides, according
to hazard from oral or dermal exposure. It also shows the criteria for a group or
class made up of compounds unlikely to present an acute hazard in normal use.
The updated WHO classification of pes- ticides by hazard can be found at a dedi-
cated web site WHO IPCS, 2006a.
Presently, WHO has classified 28 extre- mely hazardous compounds Ia, 56
highly hazardous compounds Ib, 117 moderately hazardous compounds II,
119 slightly hazardous compounds III and 248 compounds unlikely to present
Fig. 14.2. Acute toxicity of commonly used pesticides
Source: WHO IPCS 2002, EPA 2000a, b.
Table 14.1. WHO classification of pesticides according to hazard Class
Rat LD
50
mg kg BW Oral
Dermal
Solids Liquids
Solids Liquids
1a. Extremely hazardous
≤
5
≤
20
≤
10
≤
40 1b. Highly hazardous
5–50 20–200
10–100 40–400
II. Moderately hazardous 50–500
200–2000 100–1000
400–4000 III. Slightly hazardous
500 2000
1000 4000
Note. The terms solids and liquids refer to the physical state of products and formulations.
Source: WHO IPCS 2006a.
Public Health Significance of Urban Pests
489
light on the mechanism by which the pesticide causes the carcinogenic effect often accom- pany these studies. Based on study outcomes, a weight-of-evidence approach is used to
decide if a pesticide is likely to pose a cancer risk to people PMRA, 2000.
The results obtained so far by the IARC include more than 60 pesticide AIs, most of which are no longer in common use. The AIs used also for urban pest control include: the
pyrethroids deltamethrin, fenvalerate and permethrin; the organophosphates dichlorvos, malathion, methyl parathion, parathion, tetrachlorvinphos and trichlorfon; and the syner-
gist piperonyl butoxide. T hese compounds were included in IARC Carcinogen Classifications
5
Group 3 agents not classifiable as to their carcinogenicity to people, except dichlorvos, which was classified as Group 2B an agent possibly carcinogenic to
people. Among other things, dichlorvos has been criticized on the basis of biochemical and toxicological considerations FAOWHO, 1994. More recently, the Scientific Panel
on Plant H ealth, Plant Protection Products and their Residues PPR Panel of the European Food Safety Authority considered the carcinogenic potential of dichlorvos in
animals to be not relevant to human beings, on the basis of mechanistic considerations PPR Panel, 2006. Also, among the compounds used in urban pest control, dichlorvos
and pyrethrum have been reported to cause allergic contact dermatitis Moretto, 2002.
Children especially in the first 6–12 months after birth are considered by some at higher risk of toxic effects from pesticide exposure, as their metabolic processes are immature
and they are less able to detoxify chemicals. In some instances, however, metabolic imma- turity may be beneficial, because the metabolic pathways that activate their toxic meta-
bolites are not yet developed. Infants and children are growing and developing, and their delicate developmental process can be disrupted. However, the data available suggests
that this possible increased susceptibility is evident at high doses, whereas young animals do not appear to be more susceptible to low doses that cause no toxic effects in adults see
the discussion in subsection 14.3.2.2 on pyrethroids.
Exposure to pesticides during pregnancy can have potentially adverse effects on fœtal growth and child neurodevelopment Landrigan et al., 1999. However, when specifi-
cally designed studies of developmental neurotoxicity were available for approved pesti- cides, these effects were not detected at levels lower than those observed in the usual stu-
dies of developmental toxicity, multigeneration reproductive toxicity, and acute and short-term neurotoxicity. In fact, when studies with 14 pesticides evaluated by the EPA
were reviewed by JMPR, among others, the comparison of the toxicity end-points and dose levels without toxic effects that is, NOAEL or the minimal dose causing toxic
effects that is, the lowest observed adverse effect level or LOAEL of each study and of four related studies that had been performed with each chemical showed that, in gene-
ral, the NOAELs and LOAELs did not differ significantly FAOWHO, 2005.
Exposure to disrupting substances during fœtal life can also contribute to the develop- ment of a number of diseases in adult life, including cancer Birnbaum Fenton, 2003.
Pesticides: risks and hazards
488
Therefore, there might be toxicity end- points that are specific to a specific route
and duration of exposure. For instance, a dietary risk evaluation that is usually defi-
ned as the acceptable daily intake ADI will usually use an end-point from a
long-term oral feeding study, while a short-term dermal exposure risk evalua-
tion might use an acute dermal toxicity study.
Toxicity end-points discussed in this chap- ter were chosen from chemical-specific
FAOWH O Joint Meeting on Pesticide Residues JMPR assessments WH O
IPCS, 2002 and EPA regulatory end- points EPA, 2000a, b. Fig. 14.3 shows the
ADI values for some commonly used pes- ticides.
14.3.1.3. Long-term effects
