LEAD
EXPOSURE IN DEVELOPING COUNTRIES
Drs.
Mauricio Hernandez-Avila, Marlene Cortez-Lugo, Ilda Munoz,
Martha Maria Tellez, Rojo-Soliz
In humans, lead
poisoning of occupational or environmental origin may alter virtually
all biochemical process and organ systems; lead can interfere with the
reproductive and cardiovascular systems, with the blood formation process,
vitamin D function, neurological processes, among others (1). Of special
concern has been lead’s impact on the cognitive development of children
(2-5). Various studies have reported that relative small concentrations
of lead in blood are associated with persistent problems in learning
and school performance. Children with higher blood lead levels have
been shown to have lower intelligence scores than their counterparts
from a similar socioeconomic background, but with lower blood lead levels
(5). Early recognition of these toxic effects has prompted interventions
worldwide that have resulted in major reductions in lead exposure in
many countries.
In contrast with
developed countries where lead exposure is on the decline due to the
implementation of environmental and occupational regulations (1), in
developing countries lead poisoning continues to be one of the most
important problems of environmental and occupational origin (6). There
are many reasons that suggest that without proper actions lead exposure
will remain a threat to many generations of children in the developing
world (6).
Lead-intoxication
coexists with other important health problems like low immunization
coverage, malnutrition or sanitation deficiencies, which are considered
at a higher priority. In addition to the other competing health priorities,
adequate control of lead exposure is also hampered by the difficulties
experienced in implementing and enforcing new environmental and occupational
regulations. The approval and execution of new norms often face resistance
from politicians and policy makers who are more concerned about employment
figures or containment of inflation than about a clean environment.
The private sector favors low production costs at higher environmental
impacts, in order to maintain profits in a global economy. In developed
countries, organized and informed workers and groups counterbalance
resistance to new regulations. However, in developing countries these
counterbalancing forces are largely nonexistent, underdeveloped or largely
under funded. This situation has delayed the allocation of resources
needed to adequately assess, evaluate, control and prevent lead exposure
in most urban conglomerates located in these countries. In developing
countries, with the exception of leaded gasoline, most sources remain
largely understudied and uncontrolled.
Although lead exposure
is recognized as an important public health problem there are few studies
published from developing countries. Further more, most published studies
have not evaluated the effect of lead exposure among children aged six
to 24 months who are at higher risk of exposure and of suffering the
neurotoxic health effects of lead exposure. Therefore the real magnitude
of the problem remains unknown. In Table 1, we have summarized recent
published studies. Reported concentrations vary significantly between
countries, probably reflecting the different sources and the populations
selected. However, most studies show that lead continues to be a problem
in these countries. Targeting effective control measures to reduce lead
exposure will require special attention to the local patterns of exposure.
Potential sources
of lead exposure may vary within and between countries. For example
in the United States lead in paint is an important source of exposure,
while for Mexico and many other countries in Latin America this source
is largely irrelevant (1). In Mexico, food prepared in lead-glazed ceramics
is a recurrent source of exposure to lead (7), while in the United States
this source is only responsible for small limited outbreaks of lead
poisoning in children of Mexican origin (8). Therefore, in order to
develop integrated programs to control important sources of lead, it
is essential to conduct epidemiological studies to better define sources
and to assess their relative importance in order to adequately target
and evaluate interventions to reduce lead exposure.
The growing recognition
of lead’s dangerous effects has led to a worldwide initiative to reduce
lead content of gasoline (9). This initiative has already conditioned
important reductions in ambient air lead levels and population blood
lead levels. For example, in the United States the removal of leaded
gasoline from 1976 to 1991, conditioned a reduction of 78% blood lead
levels (10). In Mexico City introduction of unleaded gasoline in 1990
was associated with a decline in lead ambient concentrations from an
annual average of 1.2 ug/m3 to an annual average of 0.2 m
g/m3 in 1998 (figure 1). As expected, corresponding changes
were also observed in blood lead levels. Blood lead levels among 1st
graders children attending to the same school in the south Mexico City
have declined from 17 ug/dl in 1990 to 6.2 ug/dl in 1997 (figure 2).
Other studies have reported an estimated decline of 7.6 m g/dl
in the mean blood lead of children living in Mexico City (11).
Although blood lead
levels have declined, children born in Mexico City will still face the
risk and consequences of intra-uterine lead exposure (12). The skeleton
is the primary storage site for approximately 95 percent of lead in
the adult human body. Accumulating evidence suggests that during pregnancy
exposure to lead may increase due to the mobilization of endogenous
bone-lead stores. During pregnancy, fetal calcium requirements are met
in part through an increase in maternal bone turnover, allowing the
possibility of a greater increment in bone lead released into circulation.
Bone-lead release during pregnancy has been associated with lower birth
weights, suggesting that even at low blood lead levels, exposure may
occur due to the mobilization of endogenous lead sources. In Figure
3 we present a comparative analysis regarding bone lead levels observed
among women living in Boston, US and in Mexico City, Mexico. Recent
environmental exposure to leaded gasoline explains the higher bone lead
levels observed among Mexican women.
It is likely that
transition from leaded to unleaded gasoline will reduce lead exposure
in the population at large. However, there is concern that all internationally
supported activities will concentrate in this transition, while living
other sources of lead exposure are largely unattended. Therefore it
is important to sum up activities to control other lead sources against
those implemented and funded by initiatives related to phasing lead
out of gasoline. This is important given that as opposed to the almost
universal exposure that results from the use of leaded gasoline, that
resulting from other sources tends to be concentrated in less privileged
population living under poverty. The continued exposure to lead in these
populations perpetuates the circle of poverty and underdevelopment.
Therefore it is important to change the perception that no additional
research is needed in relation to lead epidemiology. Applied epidemiological
research within countries will be needed to characterize and control
exposure resulting from mining related activities and from informal
cottage industries that recycle batteries, fabricate ceramics or repair
radiators, among others.
Several studies
give indication of the importance of different sources. Bonilla et al
(13) in a study conducted in Nicaragua, compared blood lead levels of
children (aged 6 months to 13 years) living in the neighborhood of a
battery factory with those living in a comparable community with no
documented lead exposure. Results of this study documented that children
living close to the factory had a mean blood lead level of 17.2 ug/dl,
while children in the control community had a mean blood lead level
of 7.4 ug/dl. Similar results have been reported from Berat, Albania
(14), that children living close to a battery factory had a mean blood
lead level of 43.4 ug/dl, while comparable children of similar age living
at a distance greater than 2 km from the plant had a mean blood lead
level of 15.0 ug/dl.
Actions driven by
the findings in these studies differed, while in Nicaragua the plant
was closed, in Albania the population received advice regarding how
to avoid lead exposure. Families depending on employment in polluting
industries may have a double side impact when severe control measures
are implemented. On one side, their children may be suffering health
effects due to exposure to the toxic, while on the other, children may
suffer consequences of unemployment if the factory is closed. Current
technology allows clean production and therefore substantial reductions
in emission rates. These cases illustrate some of the complicated issues
regarding environmental control.
Other studies have
documented the impact of mining activities. In Torreon, Mexico (15)
roadside surface-dust samples from residential neighborhoods in the
vicinity of a metal smelter documented unusually high lead levels (2,448
ug/g recommended value 550 ug/g). Although these samples were collected
in 1995, the impact of this environmental exposure remained unattended
until 1999, when local newspapers reported in the issue. Recently, community
driven interest has forced the company and governmental agencies to
evaluate the problem and to initiate remedial actions for the affected
area.
Other sources of
lead exposure have been linked to cottage industry in many parts of
the world. For example backyard repair and recycling of batteries have
been documented in Jamaica (16) and Brazil (17). A recent study conducted
by Vahter et al documented this problem in the Ecuadorian Andes. The
authors studied two communities that had close to 2600 inhabitants and
whose main activity was the production of lead-glazed tiles. Tiles were
produced in about 200 family owned tile-glazing shops. Lead for glazin
was obtained from discarded car batteries. The mean blood lead levels
for children aged 4-15 years was 51 ug/dl. Children whose families were
directly involved in fabrication of tiles had a blood level of 60. ug/dl,
while those children whose families were not directly involved had a
blood lead level of 21 ug/dl. Similar, although lower levels of exposure
have been documented by Fernandez et al in Mexico. In this study children,
less than 5 years of age, whose families were involved in the fabrication
of glazed ceramics had mean blood levels of 25 ug/dl. In Mexico, lead
needed for the glaze is not obtained from car batteries, this difference
in the source of lead may explain the large observed differences in
blood lead levels in these populations.
In addition to the
different cultural patterns of manufacture of lead related products
that take place in developing countries, diet is likely to play an important
role (19,20). Lead absorption may be modulated by nutritional status.
Nutrient deficiency such as calcium, iron and zinc have been associated
with high blood lead levels (20), and several studies conducted in Mexico
City among children and women of reproductive age have shown that calcium
intake was inversely related to blood lead levels (21,22). However,
the potential therapeutic effect of dietary calcium or iron has not
yet been adequately evaluated in relation to lead absorption in human
populations(23). Further more, there is some evidence suggesting that
toxic adverse effects of lead may be more important among subjects with
iron deficiency. Iron deficiency is a prevalent condition all over the
world, but it is particularly prevalent among poor children, who are
more likely to be exposed to lead.
Control of lead
exposure in developing countries will require additional efforts to
properly target interventions to account for the particular condition
in which exposure takes place. Further research will be needed to identify
sources of lead and the populations at risk of exposure. Interventions
will need the allocation of financial resources to support targeted
screening activities, educational programs and regulatory and enforcement
actions. Interventions will also require identification and engaging
of different stakeholders. The identification and engagement of stakeholders
is a key activity for any intervention development. Decisions that are
made in collaboration and with the active participation of stakeholders
will be more effective.
Finally, it is important
to note that universal screening programs will not reduce lead exposure
unless this activity is coupled with environmental actions to reduce
lead emissions and to conduct the proper rehabilitation of affected
sites. Educational and medical interventions to reduce lead levels are
needed once the primary source has been identified and removed.
References
1.
Howson PC, Hernandez-Avila M, Rall DP. Lead in the Americas. A Call
for Action. Institute of Medicine, USA, 1995
2. Dietrich KN,
Krafft KM, Bornschein RL, Hammond PB, Berger O, Succop PA, Bier M. Low-level
fetal lead exposure effect on neurobehavioral development in early infancy.
Pediatrics 1987;80:721-730.
3. Bellinger D,
Leviton A, Waternauz C, Needleman H, Rabinowitz M. Longitudinal analyses
of prenatal and postnatal lead exposure and early cognitive development.
N Engl J Med 1987;316:1037-1043.
4. Bellinger D,
Leviton A, Rabinowitz M, Allred E, Needleman H, Schoenbaum S. Weight
gain and maturity in fetuses exposed to low levels of lead Environ Res
1991;54:151-158.
5. Banks EC, Ferreti
LE, Shucard DW. Effects of low level lead exposure on cognitive function
in children: A review of behavioral, neuropsychological and biological
evidence. Neurotoxicology 1997;18:237-282.
6.- Romieu I. Lacasana
M. McConnell R. Lead exposure in Latin America and the Caribbean. Environ
Health Persp 1997;105:398-405.
7. Romieu I. Palazuelos
E. Hernandez Avila M. Rios C. Munoz I. Jimenez C. Cahero G. Sources
of lead exposure in Mexico City. Environmental Health Perspectives.
1994;102:384-9.
8. MMWR. Lead poisoning
associated with imported candy and powdered food coloring-California
and Michigan. Morbidity and Mortality Weekly Reports 1998;47:1041-1043.
9. Lovei M., Phasing
out lead from gasoline. World Bank Technical paper no 397, 1998.
10. Pirkle JL, Brody
DJ, Gunter EW, Kramer A, Paschal DC, Flegal KM, Matte TD. The Decline
in Blood Lead Levels in the United States: The National Health and Nutrition
Examination Surveys (NHANES). JAMA. 1994;272:284-291.
11. Rothenberg SJ.
Schnaas L. Perroni E. Hernandez RM. Karchmer S. Secular trends in blood
lead levels in a cohort of Mexico City children. Archives of Environmental
Health. 1998;53(3):231-5.
12. Gonzalez-Cossio
T. Peterson KE. Sanin LH. Fishbein E. Palazuelos E. Aro A. Hernandez-Avila
M. Hu H. Decrease in birth weight in relation to maternal bone-lead
burden. Pediatrics. 1997;100:856-62.
13. Bonilla CM and
Mauss EA. A community-initiated study of blood lead levels of Nicaraguan
Children living near a battery factory. Am J Public Health 1998;88:1843-1845.
14. Tabaku A. Bizgha
V. Rahlenbeck SI. Biological monitoring of lead exposure in high risk
groups in Berat, Albania. Journal of Epidemiology & Community Health.
1998;52(4):234-6.
15. Benin AL, Sargent
JD, Dalton M, Roda S. High concentrations of heavy metals in neighborhoods
near ore smelters in Northern Mexico. Environ Health Persp 1999;107:279-284.
16 Matte TD. Figueroa
JP. Ostrowski S. Burr G. Jackson-Hunt L. Baker EL. Lead exposure from
conventional and cottage lead smelting in Jamaica. Archives of Environmental
Contamination & Toxicology. 1991;21(1):65-71.
17. Silvany-Neto
AM, Carvalho FM, Tavares TM, et al. Lead poisoning among children of
Santo Amaro, Bahia, Brazil in 1980, 1985, and 1992. Bull Pan Am Health
Organ. 1996;30:51-62.
18 Vahter M. Counter
SA. Laurell G. Buchanan LH. Ortega F. Schutz A. Skerfving S., Extensive
lead exposure in children living in an area with production of lead-glazed
tiles in the Ecuadorian Andes. International Archives of Occupational
& Environmental Health. 70(4):282-6, 1997
19. Peraza MA. Ayala-Fierro
F. Barber DS. Casarez E. Rael LT. Effects of micronutrients on metal
toxicity. Environ Health Perspect. 106 Suppl 1:203-16, 1998
20.
Mahaffey KR. Nutrition and lead: strategies for public health. Environmental
Health Perspectives. 1995;103(Suppl 6)191-196.
21.
Lacasana-Navarro M. Romieu I. Sanin-Aguirre LH. Palazuelos-Rendon E.
Hernandez-Avila M. Calcium intake and blood lead in women in reproductive
age Revista de Investigacion Clinica. 1996;48:425-430.
22.
Hernandez-Avila M. Sanin LH. Romieu I. Palazuelos E. Tapia-Conyer R.
Olaiz G. Rojas R. Navarrete J. Higher milk intake during pregnancy is
associated with lower maternal and umbilical cord lead levels in postpartum
women. Environ Res. 1997;74:116-121.
23.
Sargent JD. The role of nutrition in the prevention of lead poisoning
in children. Pediatric Annals. 1994;23:636-642.
24. Stoltzfus RJ.
Rethinking anemia surveillance. Lancet. 349:1764-6,1997.
25. Fernandez GO.
Martinez RR. Fortoul TI. Palazuelos E. High blood lead levels in ceramic
folk art workers in Michoacan, Mexico. Archives of Environmental Health.
52(1):51-5, 1997.
26. Shen XM. Yan
CH. Guo D. Wu SM. Li RQ. Huang H. Ao LM. Zhou JD. Hong ZY. Xu JD. Jin
XM. Tang JM. Umbilical cord blood lead levels in Shanghai, China. Biomedical
& Environmental Sciences. 1997;10:38-46
27. Heinze I. Gross
R. Stehle P. Dillon D. Assessment of lead exposure in schoolchildren
from Jakarta. Environmental Health
Table
I. Recent published studies describing blood lead levels among selected
population in developing countries.
|
Author
and year of publication
|
City
and country
|
Age
group
(years)
|
Population
studied
|
Sample
size
|
Sources
of exposure
identified
|
blood
levels in mg/dl
|
|
Song
HQ (1993)
|
Beijing,
China
|
5-6
|
children
|
128
|
Air
& food
|
7.7
|
|
Shen
XM (1998)
|
Shanghai,
China
|
At
birth
|
Newborns
|
348
|
Proximity
to major traffic road
Paternal
occupation
|
9.2
|
|
Heinze
I (1998)
|
Jakarta,
Indonesia
|
7
|
Schools
children
|
131
|
Leaded
gasoline
|
7.7
|
|
Hwang
YH (1990)
|
Taipei,
China
|
At
birth
|
Newborns
|
205
|
Air
Lead
|
7.4
|
|
Saxena
DK (1994)
|
Lucknow,India
|
At
birth
|
Newborns
|
|
Not
identified
|
16.9
|
|
Potula
V (1996)
|
Madras,India
|
26-55
|
Office
workers
|
10
|
Gasoline
& ambient air
|
4.1
|
|
Autoshop
workers
|
9
|
17.5
|
|
Bus
drivers
|
22
|
12.1
|
|
Traffic
police
|
88
|
11.2
|
|
Bonilla
C, 1998
|
Villa
Venezuela, Nicaragua
|
1-14
years
|
children
|
30
|
Air
lead
|
7.4
|
|
Managua,
Nicaragua
|
6months
to 13 years
|
Children
|
97
|
Living
close to a Battery factory
|
17.2
|
|
Counter
SA (1997)
|
Rural
communities
Ecuador
|
4-15
|
children
|
82
|
Recycling
of batteries
|
52.6
|
|
Schutz
A
(1997)
|
Montevideo
Uruguay
|
2-14
|
Children
|
96
|
Exposure
to traffic
|
9.5
|
|
Lopez-Carrillo
1996
|
Mexico
City
Mexico
|
1-5
|
Children
|
603
|
Ambient
air
Lead
Glazed Ceramics
|
15.0
|
|
Romieu
I
1995
|
1-5
|
Children
|
200
|
Ambient
air
Lead
glazed ceramics
|
9.9
|
|
Hernandez-Avila
1998
|
At
birth
|
Children
|
238
|
Ambient
air
Lead
glazed ceramics
|
7.1
|
|
Farias
P
1996
|
13-43
|
Pregnant
women
|
513
|
Ambient
air
Lead
glazed ceramics
|
11.08
|
|
Ramirez
AV
1997
|
Lima,
Peru
|
18-50
|
Adult
|
320
|
Degree
of industrialization
|
26.9
|
|
Huancayo,
Peru
|
22.4
|
|
La
Oroya, Peru
|
34.8
|
|
Yaupi,
Peru
|
14.0
|
|
Nriagu
J (1997)
|
Durban
Metropolitan region
|
3-10
|
Children
|
1200
|
Ambient
air
|
10.0
|
| |
Vulamehlo
South
Africa
|
3.8
|


