Doug Spilker<EMAIL_ADDRESS> 10/02/2008 03:11 PM

To

Jeanne Kasai/DC/USEPA/US@EPA

cc

Subject

Re: Mr. Spilker:  question on information you provided RE: pesticide container regs

Dear Ms. Kasai,

Sorry for the delay. I discussed your question with our attorney, and you have Bayer's permission to submit my email as you requested.

Best regards,

Doug

Doug Spilker, Ph.D.

Manager - EPA Reg. Affairs

BAYER HEALTHCARE LLC

ANIMAL HEALTH

Office: +1<PHONE_NUMBER>

Mobile: +1<PHONE_NUMBER>

Fax: +1<PHONE_NUMBER>

Email<EMAIL_ADDRESS> Address:

P.O. Box 390

Shawnee Mission, KS  66201-0390

Country: USA

Bayer Animal Health "Powered by People, Driven by Science"

<EMAIL_ADDRESS> 10/01/2008 01:38 PM

To

<EMAIL_ADDRESS> cc

<EMAIL_ADDRESS> Subject

Mr. Spilker:  question on information you provided RE: pesticide container regs

Hello, Mr. Spilker:

After the comment period closed on the proposal to amend the pesticide

container-containment regulations, you sent a note to Nancy Fitz and

myself on your request that EPA consider exempting cattle ear tags and

foil packets from labeling requirements.  (Note copied below.)

I am working on making the amendments final.  Part of the process is to

submit relevant documents to the rulemaking docket.

Because of the disclaimer on your email message, I am seeking your

permission to submit your email and the 3 pdfs you enclosed.

Thank you for your time and consideration!

Jeanne Kasai

EPA's Office of Pesticide Programs

tel.<PHONE_NUMBER>

----- Forwarded by Nancy Fitz/DC/USEPA/US on 09/15/2008 02:43 PM -----

            Doug Spilker

            <doug.spilker.b@

            bayer.com>                                              To

                                     Nancy Fitz/DC/USEPA/US@EPA

            08/25/2008 03:17                                        cc

            PM                       Jeanne Kasai/DC/USEPA/US@EPA,

<EMAIL_ADDRESS>

                                                               Subject

                                     Re: Container Disposal regs - Ear

                                     Tags exemption

Dear Ms. Fitz,

Please see the attached letter and attachments regarding this subject.

Best Regards,

Doug

Doug Spilker

Manager - EPA Reg. Affairs

BAYER HEALTHCARE LLC

ANIMAL HEALTH

Office: +1<PHONE_NUMBER>

Mobile: +1<PHONE_NUMBER>

Fax: +1<PHONE_NUMBER>

Email<EMAIL_ADDRESS> Address:

P.O. Box 390

Shawnee Mission, KS  66201-0390

Country: USA

Bayer Animal Health "Powered by People, Driven by Science"

<EMAIL_ADDRESS>

08/20/2008 12:58 PM                                                 To

                                     Doug Spilker

<EMAIL_ADDRESS>

                                                                    cc

<EMAIL_ADDRESS>

                                                               Subject

                                     Re: Container Disposal regs - Ear

                                     Tags exemption

                                                                       Hello Doug,

Your best bet would be to email the information to my colleague Jeanne

Kasai and me.  The other option is that you could submit it directly to

the docket by going to the federal regulation portal

(http://www.regulations.gov) and then submitting the comments under the

docket number for the container-containment rule (EPA-HQ-OPP-2005-0327).

The only problem is that I just went to that site to give you more

specific directions and couldn't figure out how to do it because the

comment period has officially closed.  Which is why I recommend that you

email the letter to Jeanne and me and we'll enter it into the docket.

Jeanne's email address is<EMAIL_ADDRESS> The sooner you can send that information to us, the better.  We are

working on the final rule now and are on a tight timeline to get the

final rule published by November 1, 2008.

Please let Jeanne or I know if you would like any additional

information.  Thanks!

Nancy Fitz

Office of Pesticide Programs

U.S. Environmental Protection Agency

(703) 305-7385 (phone)

(703) 308-2962 (fax)

<EMAIL_ADDRESS>(e-mail)

Pesticide storage & disposal web site:

http://www.epa.gov/pesticides/regulating/storage.htm

           Doug Spilker

           <doug.spilker.b@

           bayer.com>                                              To

                                    Nancy Fitz/DC/USEPA/US@EPA

           08/19/2008 12:18                                        cc

           PM

                                                              Subject

                                    Container Disposal regs - Ear

                                    Tags exemption

Hi Nancy,

As we discussed,  I would like to comment on the proposed regs, even

though the docket has closed.  What would be the best way - respond

directly to you or whom?  I have a couple of pictures to include as

well.  Our position will be to request the Agency to consider cattle ear

tags as one-time use products, and the foil packets (pouches) and

packaging be considered similar to the exemptions for pet collars and/or

the foil packets for other single use products.

Can you give me guidance on how to send in the information?

Thanks,

Doug

Doug Spilker

Manager - EPA Reg. Affairs

BAYER HEALTHCARE LLC

ANIMAL HEALTH

Office: +1<PHONE_NUMBER>

Mobile: +1<PHONE_NUMBER>

Fax: +1<PHONE_NUMBER>

Email<EMAIL_ADDRESS> Address:

P.O. Box 390

Shawnee Mission, KS  66201-0390

Country: USA

Bayer Animal Health "Powered by People, Driven by Science"

The information contained in this e-mail is for the exclusive use of the

intended recipient(s) and may be confidential, proprietary, and/or

legally privileged.  Inadvertent disclosure of this message does not

constitute a waiver of any privilege.  If you receive this message in

error, please do not directly or indirectly use, print, copy, forward,

or disclose any part of this message.  Please also delete this e-mail

and all copies and notify the sender.  Thank you.

For alternate languages please go to http://bayerdisclaimer.bayerweb.com

(See attached file: CyLence Ultra Ear Tag Sell Sheet.PDF)(See attached

file: Co-Ral Ear Tag Sell Sheet.PDF)(See attached file: 2008-08-25 BAH


[Federal Register Volume 86, Number 31 (Thursday, February 18, 2021)]
[Notices]
[Page 10122]
[FR Doc No: 2021-03299]

-----------------------------------------------------------------------

DEPARTMENT OF HOMELAND SECURITY

Federal Emergency Management Agency

[Internal Agency Docket No. FEMA-4510-DR; Docket ID FEMA-2021-0001]

Hawaii; Amendment No. 2 to Notice of a Major Disaster Declaration

AGENCY: Federal Emergency Management Agency, DHS.

ACTION: Notice.

-----------------------------------------------------------------------

SUMMARY: This notice amends the notice of a major disaster declaration
for the State of Hawaii (FEMA-4510-DR), dated April 1, 2020, and
related determinations.

DATES:  This change occurred on January 20, 2021.

FOR FURTHER INFORMATION CONTACT: Dean Webster, Office of Response and
Recovery, Federal Emergency Management Agency, 500 C Street SW,
Washington, DC 20472,<PHONE_NUMBER>.

SUPPLEMENTARY INFORMATION: The Federal Emergency Management Agency
(FEMA) hereby gives notice that pursuant to the authority vested in the
Administrator, under Executive Order 12148, as amended, Tammy L.
Littrell, of FEMA is appointed to act as the Federal Coordinating
Officer for this disaster.
    This action terminates the appointment of Robert J. Fenton as
Federal Coordinating Officer for this disaster.

    The following Catalog of Federal Domestic Assistance Numbers
(CFDA) are to be used for reporting and drawing funds: 97.030,
Community Disaster Loans; 97.031, Cora Brown Fund; 97.032, Crisis
Counseling; 97.033, Disaster Legal Services; 97.034, Disaster
Unemployment Assistance (DUA); 97.046, Fire Management Assistance
Grant; 97.048, Disaster Housing Assistance to Individuals and
Households In Presidentially Declared Disaster Areas; 97.049,
Presidentially Declared Disaster Assistance--Disaster Housing
Operations for Individuals and Households; 97.050, Presidentially
Declared Disaster Assistance to Individuals and Households--Other
Needs; 97.036, Disaster Grants--Public Assistance (Presidentially
Declared Disasters); 97.039, Hazard Mitigation Grant.

Robert J. Fenton,
Senior Official Performing the Duties of the Administrator, Federal
Emergency Management Agency.
[FR Doc. 2021-03299 Filed 2-17-21; 8:45 am]
BILLING CODE 9111-23-P


In summary, there is little doubt that certain compound of lead are carcinogenic or at least co carcinogenic in some species of experimental animals.

Teratogenicity There is little information in the literature to suggest that lead has a teratogenic effect in man. Although there were numerous reports of a high incidence of stillbirths and miscarriages among women working in the lead trades, fetal anomalies were not de

scribed. It must also be pointed out that these women were Droba

bly exposed to much higher concentrations of lead than for occupa

tionally exposed men today. Recent literature is devoid of any references to teratogenic effects of lead in man.

In experimental animals, on the other hand, lead has been shown repeatedly to have teratogenic effects. Early studies demon

strated this in chick embryos by injection of lead into the yolk sac ( Catzione and Gray, 1941; Karnofsky and Ridgway, 1952). Tera

togenesis has also been observed in rodents. These studies were done using high doses of lead given intravenously or intraperitone

ally. For example, McClain and Becker ( 1975) used single intra

C 63 00000 00000 l l PWWWc 4 mmmmln 00000 OUTU7Ul~ r l ooln m 000 Ina3 tiOUl mlnm 000 InInn 000 CVNW 99 90 80 Percent animals with renal 50 tumors 10 1 10.1 0.2 0.5 1 2 5 ppm Dietary Pb x 1' J3 FIGURE 6 Probit Plot of Incidence of Renal Tulnors in Male Sats Source: Azar, et al. 1973 90 80 50 10 1 10 C 65 peritoneal doses of 25 to 70 mq/ kg in rats. They found that terato

logic effects occurred when administration was on day 9. Adminis

tration later in pregnancy resulted in embryotoxicity ( fetal re

sorption) but not in teratogenic effects. Carpenter and Ferm ( 1977) observed teratologic effects in hamsters following the administration of 50 mg/ kg Pb( N03) 2 intravenously on day 8. Chron

ic administration of lead in the drinking water of pregnant rats at very high concentrations ( up to 250 mg/ l) resulted in delayed fetal development and fetal resorDtion without teratologic effects ( Rim

mel, et al. 1976).

In summary, it seems that, in man, embryotoxicity precedes teratogenicity in the lead sensitivity scale. This is SupDorted by historical experience in occupationally exposed women and by animal studies.

Mutagenicity Pertinent data could not be located in the available litera

ture concerning the mutagenicity of lead.

Reproductive Effects As was indicated in the previous section, lead has been known to cause miscarriages and stillbirths in women working in the lead trades during the latter half of the 19th century and Drobably on into the early Dart of the 20th century, It is very difficult to estimate minimally toxic exposure for stillbirth and miscarriages because exposure data, e. g., PbB are lacking for women who experi

enced this Droblem. The minimally toxic Level of exDosure may actually be quite low. Lane ( 1949) reported on the outcome of 15 pregnancies incurred among 150 women working in an unspecified lead C 66 trade during World War II. Three of these women had miscarriages

an incidence seven times normal. Unfortunately the numbers were too small to be assigned statistical significance. Lead exposure was modest, air lead being 75 ug/ m3 and urinary lead excretion in men working with these women being 75 to 125 ug/ l. A more recent Japanese study also is suggestive of miscarriages occurring among women with only modest exposure ( Nogaki, 1958). These women were the wives of lead workers. Unfortunately, the actual level of lead exposure was not reported.

It has recently been reported that the incidence of premature fetal membrane rupture in term and preterm infants is much higher 30 to 50 miles west of a lead mining area of Yissouri ( 17 percent)

than in a Missouri urban area remote from lead mining activities ( 0.41 percent) ( Fahim, et al. 1976). Maternal and fetal PbSs at birth also differed significantly for normal births vs. births with premature membrane rupture. Maternal and fetal PbBs for the normal deliveries were about 14 and 4 pg/ dl, respectively, whereas they were about 26 and 13 respectively for mothers and infants with mem

brane rupture. This provocative study needs confirmation. It is difficult to understand, for example, why fetal PbB should be so much lower than maternal PbB in all groups.

There is a possibility that lead affects fertility as well as the conception. Lancranjan, et al. ( 1975) reported that signifi

cant levels of teratospermia occurred among men working in a lead storage battery factory. Their PbBs were 30 to 80 ug/ dl. Although many studies have attempted t0 correlate semen quality with fertil

ity, the extent to which abnormally shaped sperms participate' in C 67 fertilization is unclear. Experimental animal studies have shown reduced fertiiity of both maternal and paternal origin ( Stowe and Goyer, 1971).

There have been numerous conflicting reports concerning the occurrence of chromosomal aberrations in lymphocytes of lead

exposed workers ( O'Riordan and Evans, 1974; Forni, et al. 1976).

The reason for these conflicting findings is not clear. DeKnudt,

et al. ( 1977a) suggest that ancillary factors may be critical: for example, the level of calcium intake. They base this conclusion on the lack of correspondence between lead effects in two widely sepa

rated lead using plants, one being a secondary lead smelter and the other being a plant manufacturing " tin" dishes. Lead exposures were roughly comparable: PbBs were on the order of 45 100 pgidl.

Severe chromosomal aberrations were found in one plant whereas no such effects were seen in the other. They further point out that no severe aberrations have been seen in at least some animal studies in which lead exposure was' heavy and nutrition apparently adequate ( Jacquet, et al. 1977; De Knudt, et al. 1977b). The implications of chromosomal aberrations which have been reported are not known.

A recent report by Wibberley, et al. ( 1977), which demonstrates a striking increased incidence of high placental lead associated with stillbirths or congenital malformations, further suggests that a relationship exists between intrauterine exposure to lead and re

productive casualty.

Renal Effects There is considerable information in man concerning the renal effects of lead. Two distinctive effects occur in both adults and C 68 children. One, is reversible oroximal tubular damage, which is seen mainly with short term exposure. The other effect is reduced glo

merular function which has qenerally been considered to be of a slow, progressive nature.

Tubular damage is manifested as the Fanconi triad of ql_ vco

suria, hypophosphatemia with phosphaturia, and generalized amino

aciduria. The last named manifestation appears to occur more con

sistently than either glycosuria or phosphaturia. It was first described more than 20 years ago in lead smelter workers ( Clarkson and Kench, 1956). In adults, the condition probably is uncommon at PbBs below 70 ug/ dl. Thus, in a recent series of seven workers, all of whom had PbBs 70 pg/ dl, with a range of 71 109, none had amino

aciduria or qlycosuria. Significantly, five had hemoglobins below 12 g/ d1 ( Cramer, et al. 1974). Similarly, in a series of 15 infants hospitalized for lead poisoning, all havinq PbSs ) lOO ug/ dl at

entry, only three had aminoaciduria, with PbBs of 246, 299, and 798 ug/ dl ( Chisolm, 1968).

Reduced qlomerular filtration with attendant rise in serus urea concentration is generally considered to be a progressive dis

ease, implying prolonged lead exposure. It is accompanied by interstitial fibrosis, obliteration of glomeruli and vascular lesions ( Morgan, et al. 1966). It occurs at relatively low levels of lead exposure, at least relative to the levels associated with aminoaciduria. For example, in Cramer's series of seven workers,

none of whom had aminoaciduria, three had low renal clearance of inulin ( 490 ml/ min/ 1.73m2). In another study of eight men with occupational lead exposure ( PbBs = 29 98), four had reduced glomer

C 69 ular filtration rates ( wedeen, et al. 1975). Of these four cases,

one had a PbB of 48 pg/ dl at entry. The maximal PAH secretion rate ( TmPAH) was also reduced, indicating coexistent tubular damage.

Among the other three cases, two had only a marginal depression of TmPAH' From these and other studies, it appears that the kidney is sensitive to glomerular vascular damaqe, with an imprecisely known threshold for effect which may be below PbR = 50 ug/ dl.

Cardiovascular Effects Dingwall Fordyce and Lane ( 1963) reported an excess mortality rate due to cerebrovascular disease among lead workers. These workers were employed during the first quarter of the 20th century when lead exposure was considerably higher than it has been more recently. There was no similar elevated mortality among men em

ployed more recently however. Similarly, in Cooper's more recent epidemiological study there was no excess mortality attributable to stroke or other diseases associated with hypertension or vasculo

pathy ( Cooper and Gaffey, 1975; Cooper, 1978). It would appear from these studies that the vascular effects of lead only occur with heavy industrial lead exposure  probably in excess of what is encountered today.

There have been reports of heart failure ( Kline, 1960) and of electrocardiographic abnormalities ( Kosmider and Pentelenz, 1962)

attributable to lead exposure. Yowever, these cases have always involved clinical lead intoxication. It does not seem likely,

therefore, that the heart is a critical target for lead effects.

c 70 Miscellaneous Effects Sporadic reports of other biological effects of lead in man exist, but these are difficult to evaluate as to associated lead exposure. They have frequently been reoorted only at high exposure levels and only by one or two investigators. For example, Dodic,

et al. ( 1971) reported signs of impaired liver function in 11 of 91 patients hospitalized for lead poisoning. No information was pro

vided as to indices of lead exposure. Impairment of thyroid func

tion has been reported in moonshine whiskey drinkers hospitalized for lead poisoning ( Sandstead, et al. 1969). The degree of lead exposure was not clearly indicated, but it can be assumed to have been high. Intestinal colic has long been recognized as a sign of lead in industrially exposed people. It probably also occurs in children with lead poisoning. Beritic ( 1971) reported that it occurs with PbBs as low as about 40 ug/ dl. This seems unlikely since the cases he reported also were anemic, a condition associat

ed with the considerably higher PbBs. A number of studies have suggested that a relationship exists between lead exnosure and amyotrophic lateral sclerosis ( ALS). The most recent report on this examined plasma lead levels in 16 cases of ALS and in 18 con

trols and found significant differences at the 0.05 level ( Conradi,

et al. 1978).

Finally, animal studies indicate that relatively high levels of lead exposure interfere with resistance to infectious disease ( Hemphill, et al. 1971: Gainer, 1974). There are no reports of an abnormal infectious disease incidence among people with high lead exposure, however.

c 71 CRITERIOW FORYULATIOY Existing Guidelines and Standards Since lead is ubiquitous in the environment, several govern

ment agencies have become involved in regulating its use. The most recent action was taken by the Consumer Product Safety Commission ( CPSC) . In 1977 the CPSC lowered the maximum allowable concentra

tion of lead in house paint to 0.06 percent. At present the Occupa

tional Safety and Health Administration ( OSHA) is preparing a set of regulations regarding occupational lead exposure. Similarly,

the U. S. EPA has set an ambient air lead standard. The U. S. FDA has provided new guidelines for the regulation of sources of lead in foods and cosmetics. Given the multi media nature of lead exposure to man, it is essential that any action taken in regard to one source, such as water, be coordinated with similar actions being taken for other media such as air and diet.

Current Levels of Exposure Approximately 1 percent of taowater samples have been found to exceed the current standard of 50 pg/ l. This is generally a prob

lem in softwater areas, particularly where lead pipes convey the water supply to the tap from the surface connection. The contri

bution of the diet is approximately 200 pq/ day for adults. For children ( ages three months to nine years) the diet contributes 40 to 200 ug of lead per day. On the basis of current information, it is impossible to judge how much dietary lead is attributable to the water used in food preparation. The concentration of lead in ambi

ent air ranges from approximately 0.1 ug/ m3 in rural areas to as much as 10 us/ m' in areas of heavy automotive traffic.

C 72 Special Groups at Risk In addition to these usual levels of exposure from environ

mental media, there exist miscellaneous sources which are hazard

ous. The level of exposure resulting from contact is highly vari

able. Children with pica for paint chips or for soil may experi

ence elevation in blood lead ranging from marginal to sufficiently great to cause clinical illness. Certain adults may also be ex

posed to hazardous concentrations of lead in the workplace, notably in lead smelters and storage battery manufacturing plants. Again,

the range of exposure is highly variable. Women in the workplace are more likely to experience adverse effects from lead exposure than men due to the fact that their hematoDoietic system is more lead sensitive.

Basis and Derivation of Criterion The approach that will be taken here in assessing the impact of lead in water on human health is basically the same as has been taken by the U. S. EPA ( 1977) for lead in air. The critical target organ or system must first be identified. Then, the highest inter

nal dose of lead that can be tolerated without injury to the tarqet organ must be specified. Finally, the impact of lead in water on the maximum tolerated internal dose must be estimated, as well as the likely consequences of specific reductions in the maximum allowable concentrations of lead in water.

In identifying the critical organ or system, great reliance is placed on the concentration of lead in the blood ( PbB) as an index of internal dose. Such an indirect measurement is necessary be

cause of the multi media character of lead intake. Tt is virtually c 73 impossible to measure total lead intake in People in any meaningful way. Because intake and output fluctuate greatly from day to day,

measurement of total lead intake would reauire long term balance studies. Variables have a substantial influence on the rate and degree of lead uptake from the external environment. Some groups have proposed alternatives to PbB as a measure of internal dose,

e. g., FEP and tooth lead. FEP is not suitable because it is a bio

logical response to lead. As such, it is subject to influences other than lead, notably iron deficiency. Tooth lead is a poten

tially useful index of lead exposure, but with the present state of the art being what it is, tooth lead is difficult to internret. It only provides an integrated profile of past lead exposure. One is not able to say when the exposure occurred. It has the additional limitation of not being available on demand. Teeth are shed spon

taneously only in childhood. Yoreover, only a very small data base is available for dose effect and dose response using any measure of dose other than PbB. The use of PbR as a measure of internal dose is widely accepted, simply because nothing better is available.

Having specified that PbB is the best measure of internal dose currently available, the next question concerns the lowest PbB lev

els at which adverse health effects occur. Two recent documents ( U. S. EPA, 1977; WHO, 1977) have been oublished in which iudgments were rendered in this regard ( Table 12). It will be noted that the estimates are strikingly similar. The estimated no effect levels are based on limited populations and probably are lower to some undefinable degree in the total population at risk. Slightly more information was available to the U. S. E? A panel than to the WI0 L c 74 TABLE 12 Summary of Lowest PbBs Associated with Observed Biological Effects in Various Ponulation Crouosa Lowest Observed Effect Level ( pg Pb/ lOO ml Blood) Effect Population Grouu 10 15 20 25 30 40 40 40 50 50 60 50 60 80 100 100 120 ALAD inhibition Erythrocyte protoporbhyrin elevation Erythrocyte protoporohyrin elevation Increased urinary ALA excretion Anemia Coproporphyrin elevation Anemia Cognitive ( CNS) deficits Peripheral neuropathies Encephalopathic symptoms Encephalopathic symptoms Children and adults Women and children Adult males Children and adults Children Adults and children Adults Children Adults and children Children Adults No Observed Effect Levels in Terms of PbBb No Observed Effect Level ( pg Pb/ lOO ml Blood) Effect Population Group 10 Erythrocyte ALAD inhibition 20 25 FEP 20 30 FEP 25 35 FEP 30 40 Erythrocyte ATPase inhibition 40 ALA excretion in urine 40 CP excretion in urine 40 Anaemia 40 50 Peripheral neuropathy 50 Anaemia 50 60 Minimal brain dysfunction 60 70 Minimal brain dysfunction 60 70 Encephalopathy 80 EncePhalopathv Adults and children Children Adult females Adult males General Adults and children Adults Children Adults Adults Children Adults Children Adults aSource: U. S. EPA, 1977 b Source: World Health Organization, 1977 c 75 panel since it reviewed literature through mid 1977, whereas the WHO expert groups reviewed literature only through 1976. In addi

tion, the U. S. EPA performed statistical calculations based on the known distribution of blood lead levels in the United States.

Both sets of data in Table 12 are in error in one regard. They use the term " anemia" inappropriately under the " Effect" column.

What they really mean is " decrement in hemoglobin." Anemia is a clinical term used to denote a degree of hemoglobin decrement which is below the normal range for that class of individuals, e. g., men or children.

The question that arises in considering Table 12 is which is the critical effect? Precisely the same issue confronted the U. S.

EPA in its deliberations concerning establishment of a national ambient air quality standard for lead ( 42 FR 630979). It focused on the lead effects in children since they are more sensitive than adults.

It ruled that the maximum safe blood lead level for any given child should be somewhat lower than the threshold for a decline in hemoglobin level ( 40 ug Pb/ dl). In considering how much lower this limit should be, the U. S. EPA cited the opinion of the Center for Disease Control, as endorsed by the American Academy of Pediatrics,

that the maximum safe blood lead level for any given child should be 30 pg/ dl. Based upon epidemiological and statistical considera

tions, the U. S. EPA estimated that if the geometric mean PbB were kept at 15 pg/ dl, 99.5 percent of children would have PbB L30 w/ dl. This position provides a substantial margin of safety which accomodates minor excursions in lead exoosure due to adventitious C 76 sources. Controls on lead in obligatory media ( e. g., air and water) do not protect children from the hazards of pica for lead

base paint chips or soil and dust contaminated with lead from such sources as fallout from the smoke zone of lead smelters.

In its deliberations concerning an ambient air lead standard,

the U. S. EPA estimated that the contribution of sources other than air to PbB is i0 to 12 ug/ dl. This is bresclmably composed over

whelmingly of dietary sources which, in turn, is composed of both food and water.

The next question concerns the contribution of water to lead exposure. Only three useful studies of the interrelationship be

tween PbB and lead in drinking water are available. Overall, the Moore, et al. ( 1977a) study, the one by Hubermont, et al. ( 1978),

and the calculations made from U. S. EPA data collected in the Boston area ( Greathouse and Craun, 1976) are credible because they are consistent with other information concerning the curvilinear relationship between 2bB and air Pb. The implication of the equa

tion describing the relationship between PbB and water lead is that with increasing lead in water, the incremental rise in PbB becomes progressively smaller, as with air lead vs. ? bB and dietary lead vs. PbB ( see " Contributions of Lead from Diet vs. Air to PbB" in the Pharmacokinetics section). The water lead vs. PbB relationship differs in one significant respect, however, from the air lead vs.

PbB relationship in that the baseline PbB ( 0 water PbB) is indepen

dent of the contribution of water lead to PbB. Thus, regardless of whether one starts with a baseline PbB of 11 ug/ dl, as was indicat

ed in the Moore, et al.. ( 1977a) study or whether one starts at some c 77 other PbB level, e. g.) 20 ug/ dl, the add on PbB from any given level in water will be the same. Such is not the case in the Azar analysis of air Pb vs. PbB ( see " Contributions of Lead from Diet vs. Air to PbB" in the Pharmacokinetics section). Here, the higher the baseline, the less is the contribution of air Pb. This is be

cause log PbB is proportional to baseline PbB + log air concentra

tion. Future research may provide better insiqht into whether this discrepancy is real and, if so, why. The question is of some prac

tical importance. For instance, if you have a baseline PbB ( no lead in water) of 30 pg/ dl, such as in a child acquiring lead from paint, it would be of some importance to know whether an additional increment of lead in water would have the same impact on PbB as it would in a child having a baseline of PbB of 10 pg/ dl. An Azar type model would suggest a lesser impact starting from the higher base

line PbB.

So far as a specific recommendation regarding a water auality for Pb is concerned, a stand must be taken using the available data. Beginning with the assumption that a PbB of 12 ug/ dl is essentially attributable to food and water and that the average lead content of water consumed is 10 ug/ l, aporoximately 5 ug Pb/ dl blood ( from Table 6) is attributable to the water that is used in food and beverage preparation and in direct consumption. If the water Pb were consistently consumed at the present Pb standard of 50 ug/ l instead of at 10 pg/ l, an additional contribution of ap

proximately 3.4 uq/ dl to PbB would result ( 3.57  5.13 from Table 6) l This would yield a. total PbB of 12 + 3.5 or 15.4 pg/ dl, the approximate maximum qeometric mean PbB compatible with keeping 99.5 C 78 percent of the population under PbB = 30 ug/ dl. Thus, based on most recent data, the present water standard of 50 ug Pb/ l may be viewed as representing the upper limit of acceptability. This criteria is based on empirical observation of blood lead in human population groups consuming their normal amount of water and food daily. Spe

cific amounts of foods or drinking water consumed were not quanti

fied, but it can be assumed that they reflect an average consump

tion of water, fish, shellfish, and other foods.

All the assumptions that have been made in arriving at an estimate of the impact of lead in water on PbB have been on the conservative side. For instance, unpublished data from the Com

mission of the European Communities suggest that the impact of lead in water on PbE is appreciably less than has been estimated from published data used in this document [ personal communication from Alexander Berlin, et al. ( 19781, Commission of the European Com

munities, 1 Luxembourg] . Furthermore, data from a study ( Morse, et al. 1978) of the effect of lead in water on the PbB of a population of children in a relatively small town are reassuring, They indi

cate that among children whose water supply contained 50 to 180 ug Pb/ l, PbBs averaged 17.2 ug/ d12.

1 Subsequent to the writing of this reoort, these data were submit ted to the EPA by Dr. Berlin. They were studied and judged not to alter the conclusions arrived at in this document concerning PbB vs. lead in water ( see Appendix). 2 It should be pointed out, however, that the contribution from other sources is not indicated, thus, the relative water lead con tribution is unknown.

c 79 Finally, there remains the issue of the carcinogenic effects of lead. Using data from one species of laboratory animal ( the rat) it was possible to construct a seemingly valid dose response curve and to calculate a dietary level of lead which would predict an incidence of cancer in l: lOO, OOO peoole. This calculated diet

ary level of lead is 29 ug/ kg. Since this estimate includes lead from all sources, its implications are beyond the scone of this document. It should be noted, however that the International Agency for Research on Cancer, Lyon, France considers the exneri

mental animal evidence to be of dubious significance with regard to man ( IARC, 1972).

The Agency has not yet resolve all of the issues concerning the potential carcinogenicity of lead, but will complete its review in the near future. All of the data will be subjected to an exten

sive peer review by outside experts and in house scientists. De

pending upon the final conclusions of the review, the water quality criteria for lead may be re evaluated. REFERENCES Albert, R. E., et al. 1974. Follow up of children overexposed to lead. Environ. Health Perspect. Exp. Issue No. 7: 33.

Alexander, F. W., et al. 1973. The Uptake and Excretion by Chil

dren of Lead and other Contaminants. In: Proc. Int. Symp. Environ.

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c 103 APPENDIX*

Results of the research examined in the Commission of the European Communities ( CEC) paper are summarized in Tables 1 and 2.

The data presented in Table 1 are equations developed by the auth

ors concerning the relationship of blood lead ( PbB) to water lead ( PbW). Table 2 consists of calculations of the contribution of 100 µ g Pb/ l of water to PbB ( as µ g/ dl). Some of these calculations were made by Berlin, et al. ( 1978), interpolating from data points in the articles cited. Others were made using the equations provided by the authors of the articles cited.

Three types of equations are presented:

( 1) PbB = a + b PbW ( 2) PbB = a + log PbW ( 3) PbB =

In all cases " a" is the baseline expressing PbB at PbW = 0. Of these three mathematical relationships, the third appears to be the most valid for two reasons: ( 1) the largest number of subjects are involved in studies using this equation, and ( 2) it corresponds to the analysis of U. S. EPA data ( Greathouse and Craun, 1976) as cited in the lead criterion document, which also involved a very large number of subjects. Moreover calculations made of PbB vs. PbW using the U. S. EPA data were for females aged 20 to 50, a sub popu

lation which probably gets a larger proportion of its water from * Summary of " Research of PbB vs. Lead in Drinking Water in Europe" as presented by A. Berlin, et al. ( 1978), Commission of the European Communities.

C 104 TABLE 1 Relationships between PbW and PbB*

Relationship Remarks Reference PbB = 0.018 PbW + 22.9 = 0.417 Pbw = µ g/ l PbB = µ g/ l00 ml First morning flush Addis and Moore, 1974 PbW and PbB in µ mol/ l Moore, 1977a PbB = 0.76 + 0.15 PbW r = 0.58, first morning flush PbB = 0.80 + 0.20 Pbw r = 0.52, running sample PbW and PbB in µ mol/ l Moore, et al. 1977 PbB = 0.533 + 0.675 3 Pbw first morning flush PbB = 0.304 + 1.036 3 Pbw running sample PbW in µ g/ l PbB in µ g/ 100ml Lauwerys, et al. 1977 PbB = 9.62 + 1.74 log Pbw first morning flush PbW and PbB in µ mol/ l PbB = 0.8 + 0.19 PbW first morning flush Moore, 1977b PbB = 0.8 + 0.53 PbW full flush ( paired samples)

PbB = 19.6 + 7.2 PbW PbW in ppm, PbB in µ g/ l00ml first morning flush Elwood, et al. 1976 PbB = 20.7 + 12.6 PbW As above. Beattie, et al. 1976 Re evaluated data * Source: Berlin, et al. 1978 C 105 TABLE 2 Increment in PbB for an Increase of 100 ~ g/ l in PbW ( for Concentrations around 100 llq/ l)*

Increment in PbR Remarks Reference 1.3 ~ g/ lOOml For running sample ( linear interpolation) 20 1040 pg/ l PbW 1.2 pq/ lOOml First flush ( linear inter polation) lo 250 pg/ l PbW 3.4 c1q/ lOOml For running sample ( linear interpolation) lo 250 pg/ l PbW 3.3 lig/ lOOml For first flush ( linear inter polation) 35 350 ug/ l PbW De Graeve, et al. 1975 Beattie, et al. 1972 Covell, 1975 Addis, et al. 1974 I.. 8 ~ g/ lOOml Using the linear equation derived by the authors Addis, et al. 1974 2.0 pq/ lOOml Using the linear equation derived by the author for running water samples. Moore, 1977a 6.0 pq/ lOOml Using the non linear equation derived by the authors for running water samples. Moore, et al. 1977 3.9 lig/ lOOml Using the non linear equation de rived by the authors for first morning flush. Moore, et al. 1977 0.83 J~ g/ lOOml IJsing the log equation derived by the authors Lauwerys, et al. 1977 In view of the low PbW value, the extrapolation is uncertain. vos, et al. 1977 C 106 TABLE 2 ( Continued)

Increment in PbB Remarks Reference 1.9 pg/ lOOml Using the linear equation derived by the authors for morning flush Moore, et al. 1977 5.3 pg/ lOOml Using the linear equation derived by the authors for full flush Moore, et al. 1977 0.72 pg/ lOOml Using the linear equation derived by the authors for morning flush. Elwood, et al. 1976 1.3 pg/ lOOml Using the re evaluated linear equation derived by the authors for morning flush. Beattie, et al. 1976 * Source: Berlin, et al. 1978 c 107 the domestic supply than the population at large. In that regard,

the only comparable population was 70 pregnant female subjects in the study of Hubermont, et al. ( 1978) cited in the CEC document as Lauwreys, et al. ( 1977).

In summary, of the studies cited in the CEC document, most weight should probably be given to the Moore, et al. ( 1977a) cita

tion, on the basis of large numbers of samples of water and study subjects, and to the Hubermont, et al. ( 1978) study on the basis of a substantial number of subjects which were probably partaking of more of the domestic water supply than other sub classes by virtue of pregnancy and sex.

So far as the actual calculations in Table 2 are concerned,

there is one error. The CEC document calculates that the equation of Hubermont, et al. ( 1978) ( cited as Lauwreys, et al. 1977) would predict that PbW at 100 F. rg/ l would result in a PbB contribution of 0.83 pg/ dl. The error is obvious. In the equation, the PbB contri

bution of water is given by PbB = 1.74 log PbW. In fact, 0.83 =

1.74 log 3, not 1.74 log 100. The correct calculation is PbB =

1.74 x 2 = 3.48, since log 100 = 2.

Of the 13 estimates of PbB vs. PbW in Table 2, only 5 could be verified. These were Addis, et al. ( 1974) ( interpolation), Addis,

et al. ( 1974) using authors' equation, Voore ( 1977a) using author's equation, Beattie, et al. ( 1976) using author's equation, and Moore, et al. ( 1977), non linear morning flush. Of the remaining nine, one was miscalculated by CEC and the remaining eight could not be verified by this author because the oaper was unavailable ( Covell, 1975; Elwood, 1976), or because the necessary data were C 108 not in the paper ( De Graeve, et al. 1975; Yoore, et al. 1977 using non linear equation for running water; Moore, et al. 1977 using linear equation for morning flush and running water calculations),

or because it was not possible to see how CEC made an interpolation from the data cited ( Beattie, et al. 1972).

In summary, the two most credible studies among the nine actu

ally scrutinized in this addendum were the very ones utilized in the criterion document for lead. Of the two reviewed by the CEC but not examined at the time of this writing ( Covell, 1975; Elwood,

1976), one was reviewed prior to development of the criterion docu

ment and rejected on the basis of the seemingly inappropriate use of a linear regression model ( see " Contributions of Lead from Diet vs. Air to PbB" in the Pharmacokinetics section). It is therefore concluded that information provided by CEC does not alter the eval

uations made in the criterion document.

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* U. S. KWSXMFXT PRINTINQ OFFICE: 1980 0 7ZC 016/ 5960 c 111