Human immunodeficiency virus (HIV) infects CD4+ lymphocytes, leading to a development of malignant lymphomas, such as HIV‐associated Hodgkin Lymphoma (HIV‐HL). This study aimed to assess the differences in cellular composition of the inflammatory reactive background of HIV‐HLs. We examined infiltrating T lymphocytes, specifically regulatory T cells, cytotoxic cells, Epstein‐Barr virus (EBV) related antigens and HIV‐receptor CCR5. In all HIV‐HL cases, Hodgkin and Reed‐Sternberg (HRS) cells showed EBER1 expression, LMP‐1 staining positivity and EBNA‐2 staining negativity, except for one case which showed LMP‐1 staining negativity. Our histological findings indicate the percentage of CD8+, TIA‐1+ lymphocytes was significantly higher in HIV‐HL than in non‐HIV‐HL cases (P < 0.05). On the other hand, the percentage of CD4+, FOXP3+ lymphocytes was significantly lower in HIV‐HL than in non‐HIV‐HL cases (P < 0.05) but present. The percentage of CCR5+ lymphocytes was significantly lower in HIV‐HL than in non‐HIV‐HL cases (P < 0.05). Usually, CD4+ and CCR5+ lymphocytes are reported to be rarely detected in HIV‐associated non‐Hodgkin lymphomas, but the presence of CD4+ and/or FOXP3+ lymphocytes may be implicated in the pathogenesis of HL. In addition, although additional CD8+ lymphocytes are probably not EBV‐LMP specific cytotoxic T‐cells, these lymphocytes may also well be involved in the pathogenesis of HIV‐HL.

To the Editor: Juvenile myelomonocytic leukemia (JMML) is a rare pediatric hematopoietic malignancy that accounts for less than 2% of all childhood leukemias. The World Organization Health Classification defines JMML as a myelodysplastic/ myeloproliferative neoplasm (MDS/MPN) and the main diagnostic criteria is as follows: peripheral blood monocytosis >1 ¥ 10/L; blasts (including promonocytes) account for <20% of the leukocytes in the blood and of the nucleated bone marrow cells; no Philadelphia (ph) chromosome or BCRABL1 fusion gene; increased HbF levels; immature granulocytes in the peripheral blood; and granulocyte-macrophage colony-stimulating factor (GM-CSF) hypersensitivity of myeloid progenitors in vitro. On one hand, although JMML criteria for a definite diagnosis specifies GM-CSF hypersensitivity, the clinical significance of cytokines has remained unknown. On the other hand, in adult chronic myelomonocytic leukemia (CMML), which has many similarities with JMML, interleukin-6 (IL-6) and several cytokines are associated with the activity of myelomonocytic leukemic cells. Herein we report an autopsy case of a 2-month-old girl with JMML who developed multiple organ infiltration including infrequently infected regions. She was brought by her parents to her family doctor’s clinic with a complaint of poor suckling, and was incidentally found to have hepatosplenomegaly, leukocytosis with monocytosis, anemia, and thrombocytopenia. When she was admitted to our hospital, her white blood cell and peripheral blood monocyte counts were 24 ¥ 10/L and 7.6 ¥ 10/L, respectively. Peripheral blood smear obtained on admission revealed an increase in atypical monocytoid cells (Fig. 1a), and myeloid precursors were present. Myeloblasts, promyelocytes, myelocytes, and metamyelocytes were detected in 9.6%, 0.6%, 2.0%, and 1.8%, respectively. The bone marrow smear was hypercellular with granulocytic proliferation. Blasts including promonocytes of the leukocytes in the blood and of the nucleated bone marrow cells were 18.8% and 3.4%, respectively. The HbF level was 9.5%. The cytogenetic findings were normal and neither Ph chromosome nor BCR-ABL rearrangement was observed. The patient was therefore diagnosed with JMML and given a maintenance therapy consisting of transfusion and chemotherapy (6-MP). However, she deteriorated into respiratory failure in parallel with marked leukocytosis (WBC 90 x10/L) and died one month after the diagnosis. Post-mortem examination was performed 5 h after the patient’s death. The macroscopic findings were that body development was delayed (height: 56 cm,—0.54SD; weight: 6.7 kg,—0.88SD) and there was no evidence of Noonan’s syndrome or neurofibromatosis. Hepatomegaly and splenomegaly were conspicuous, with the liver weighing 350 g (standard weight: 205 g) and the spleen 260 g (standard weight: 13 g). The cut surface of the lungs showed almost no inflation and severe congestion. Multiple small and sporadic nodular lesions were seen in the bilateral lobes. The kidneys were enlarged with severe congestion, and both of them weighed 29 g (standard weight: 19 g). Erosive lesions and small nodular lesions were observed in the mucosa of the small intestine and colon. Multiple hilar lymph nodes were swollen, while the thyroid gland showed no significant abnormalities. Microscopic examination of the bone marrow specimen showed massive infiltration of atypical monocytoid cells (Fig. 1b). These cells stained positive for the antibodies of CD68, Lysozyme, CD163, MPO and negative for CD34, c-kit, CD20, CD3, suggesting that they were myelomonocytic leukemic cells. Although a small number of leukemic cells on admission were positive for the antibodies of IL-6 in the blood and bone marrow (7% and 3%, respectively), the positivity of leukemic cells at autopsy was much higher (about 80%) (Fig. 1c,d). The cavity of the bilateral lungs appeared to be the result of a massive collapse due to the infiltration of leukemic cells. However, no evidence was detectable of a virus or bacteria in the respiratory organs. Infiltration by monoleukemic cells was also pronounced in the spleen, liver, kidney, digestive tract, thyroid gland, and hilar lymph nodes (Fig. 2). Acute respiratory failure because of massive infiltration of leukemic cells, which generally accounts in part for mortality, was regarded as the main cause of the patient’s death. Clinically, JMML is well known to be associated with organ infiltration, such as spleen and liver, and the other common exogenous infiltration sites are lung and skin. However, most of these involvements have been reported as manifestations, observed in isolated biopsies. To the best of our knowledge, the regions of infiltration seen in our case, the kidney, thyroid glands, digestive tract, and lymph nodes, Pathology International 2010; 60: 333–335 doi:10.1111/j.1440-1827.2010.02517.x

Angioimmunoblastic T-cell lymphoma (AITL) is a peripheral T-cell lymphoma characterized by systemic disease with polymorphous infiltrate including macrophages. Although many studies of tumor-associated macrophage (TAM) populations in various malignant tumors have been published, only a few have dealt with activation of macrophage phenotypes such as M1 and M2 in tumor tissue. Because M2 macrophages highly express CD163, we suspected that CD163 may be a useful marker for identification of activation of macrophage phenotypes in AITL. We performed a retrospective study of immunohistochemical expression using two markers for macrophages [CD68 (PG-M1), CD163] and of the correlation of these expressions with overall survival of 42 AITL patients. The number of CD68-positive cells in AITL tissues did not correlate with overall survival (P= 0.59), whereas the number of CD163-positive cells and overall survival correlated to some extent (P= 0.08). Meanwhile, a higher ratio of CD163-positive to CD68-positive cells in AITL significantly correlated with worse overall survival (P= 0.036). Considering that this ratio reflects the proportion of macrophages polarized to the M2 phenotype, our findings indicate that activation of macrophages towards the M2 phenotype correlates with worse prognosis. Our findings indicate that the ratio of M2 macrophages expressed may be a useful marker for prognosis of AITL.

Only a few reports have described regression of rectal mucosa-associated lymphoid tissue (MALT) lymphoma after antibiotic treatment are generally found to be successful for gastric tumors. We examined eight rectal MALT lymphomas treated with antibiotic treatments to determine whether they regressed after treatment. We also discuss the relationship between rectal MALT lymphomas and MALT1 gene genetic abnormalities. Eight patients who had undergone antibiotic treatments were followed up with colonoscopy after initiation of the treatment. In five of the eight cases (63%) endoscopic examination showed that the rectal tumor had disappeared, which was confirmed histologically. Polymerase chain reaction for immunoglobulin heavy chain identified a monoclonal band in seven of eight cases (88%). Of the eight cases analyzed with fluorescence in situ hybridization (FISH) for MALT1 translocation, two demonstrated MALT1 gene genetic abnormality. These cases tended to be resistant to antibiotic treatment. Investigation and analysis of a large number of rectal MALT lymphomas are needed to establish suitable standards for antibiotic treatment.

( Cancer Sci 2010; 101: 806–814) Although the 2008 World Health Organization classification defines two subtypes of mantle cell lymphoma (MCL), classical and aggressive, we often encounter MCL with both features in the same site. We named this feature "MCL with focal aggressive form (intermediate MCL)”. In the present study, we reclassified 237 patients with cyclin D1 (CCND1)‐positive MCL on the basis of the concept of intermediate MCL, and analyzed the correlation of this reclassification with immunohistochemical detection of CCND1, Ki‐67, p53, p27 Kip1 , and p21 WAF/Cip1 . The median overall survival was 77, 31, and 18 months for classical, intermediate, and aggressive MCL, respectively, showing a statistically significant difference ( P < 0.0001). The expression levels of CCND1, Ki‐67, p53, and p21 WAF/Cip1 in aggressive MCL (mean 80.1 ± 27.8%, 73.7 ± 28.9%, 31.0 ± 69.0%, and 10.4 ± 24.8%, respectively) were higher than those in classical MCL (mean 58.1 ± 36.7%, 25.2 ± 25.5%, 6.5 ± 24.3%, and 2.5 ± 13.0%, respectively) and intermediate MCL (mean 75.7 ± 31.4%, 30.8 ± 33.3%, 21.0 ± 57.4%, and 4.8 ± 16.5%, respectively). Significantly different levels of Ki‐67 and p21 WAF/Cip1 were only recognized between intermediate and aggressive ( P < 0.05 and P < 0.0001, respectively), whereas those of CCND1 and p53 were only between classical and intermediate ( P < 0.0001 and P < 0.05, respectively). There were no significant differences in p27 Kip1 among the three groups. The subsequent discriminant analysis with independent prognostic factors clearly demonstrated that the morphological evolution of MCL occurs in parallel with increased labeling index of CCND1 and Ki‐67. The diagnosis of intermediate MCL thus proved to be of major significance and should enable the design of more tailored therapies.

Macrophage polarization is divided into M1 and M2 type based on membrane receptors, cytokines, and chemokines. M1 expresses CD80, interleukin (IL)‐6, IL‐12, and chemokine receptor (CCR)7, while M2 expresses CD163, IL10, and chemokine ligand (CCL)22. The aim of the present study was to identify the properties of infiltrating tissue macrophages in histiocytic necrotizing lymphadenitis (HNL). Twenty patients with HNL were studied, and immunohistochemistry for CD68 (KP1), CD163, CCL22, CCR7, and CD123 was done, along with myeloperoxidase (MPO). To evaluate the phenotypes of tissue macrophages in HNL, the number of cells stained positively for CD163, CCL22, CCR7, CD123 and MPO concurrently with CD68 was counted, and the ratio was calculated for each antibody to CD68+ cells. There was a high rate of co‐expression for CD163 (median, 78%) or CCL22 (80%) and a low rate for CCR7 (5%) in CD68+ cells. It is therefore conceivable that infiltration by M2 macrophages is dominant in HNL. Furthermore, some CD68+ tissue macrophages in HNL co‐express MPO or CD123 (range, 5–80%; median, 23% and 40%, respectively). It is suggested that these characteristic tissue macrophages may be associated with the pathogenesis of HNL and that M2 macrophages may infiltrate to repair the lymphoid tissue injured by cytotoxic T cells in HNL.

Macrophage polarization is divided into M1 and M2 type based on membrane receptors, cytokines, and chemokines. M1 expresses CD80, interleukin (IL)-6, IL-12, and chemokine receptor (CCR)7, while M2 expresses CD163, IL10, and chemokine ligand (CCL)22. The aim of the present study was to identify the properties of infiltrating tissue macrophages in histiocytic necrotizing lymphadenitis (HNL). Twenty patients with HNL were studied, and immunohistochemistry for CD68 (KP1), CD163, CCL22, CCR7, and CD123 was done, along with myeloperoxidase (MPO). To evaluate the phenotypes of tissue macrophages in HNL, the number of cells stained positively for CD163, CCL22, CCR7, CD123 and MPO concurrently with CD68 was counted, and the ratio was calculated for each antibody to CD68+ cells. There was a high rate of co-expression for CD163 (median, 78%) or CCL22 (80%) and a low rate for CCR7 (5%) in CD68+ cells. It is therefore conceivable that infiltration by M2 macrophages is dominant in HNL. Furthermore, some CD68+ tissue macrophages in HNL co-express MPO or CD123 (range, 5-80%; median, 23% and 40%, respectively). It is suggested that these characteristic tissue macrophages may be associated with the pathogenesis of HNL and that M2 macrophages may infiltrate to repair the lymphoid tissue injured by cytotoxic T cells in HNL.

The aim of the present study was to identify the mechanism of hepatocellular apoptosis induced by EBV‐infected cytotoxic T/natural killer (NK) cells in chronic active EBV infection (CAEBV). Eight patients with CAEBV were studied, and infected T‐cell expansion and NK‐cell expansion were detected in four patients each. Biopsy or necropsy was performed on lymph node, liver, or spleen, and each specimen was subjected to immunohistochemical double staining of CD3 plus caspase‐3 with the addition of cytotoxic markers of T‐cell restricted intracellular antigen‐1 (TIA‐1), perforin, and granzyme B, as well as EBV in situ hybridization (EBV‐ISH). In the liver, some of the infiltrating CD3‐positive lymphocytes stained positively for EBV‐ISH and cytotoxic markers. Double staining of CD3 plus caspase‐3 indicated caspase‐3 positive hepatocytes with apoptotic features, accompanied by extensive infiltration of CD3‐positive cells, which were directly attached to the apoptotic caspase‐3 positive hepatocytes. In contrast, far fewer cells stained positive for caspase‐3 in lymph node and spleen than in liver. The present findings suggest that in patients with CAEBV, cytotoxic T/NK cells may directly induce hepatocytes to undergo apoptosis more frequently than they do cells in other organs of the reticulo‐endothelial system.

Although various CD markers have been analyzed in T‐cell and natural killer (NK)‐cell lymphomas, the sensitivity and specificity of these phenotypic features have not been satisfactorily characterized. Flow cytometry (FCM) was used to determine the phenotypic pattern of 490 T/NK‐cell lymphomas with the aid of a set of surface antigens (CD2, CD3, CD4, CD5, CD7, CD8, CD10, CD11c, CD16, CD19, CD20, CD25, CD30, CD34, and CD56). In data obtained from 319 patients, CD10 expression was detected in 57% of angioimmunoblastic T‐cell lymphomas, CD30 in 93% of anaplastic large cell lymphomas, CD34 in 50% of lymphoblastic lymphomas, and CD56 in 100% of extranodal NK/T‐cell lymphomas nasal type. A total of 92% of adult T‐cell leukemia/lymphomas (ATLL) had expression of CD25 and downregulation of CD7. Of special interest is that 92 ATLL (50%) were CD4+CD7‐CD25+ phenotype while only four peripheral T‐cell lymphoma unspecified (9%) and one (9%) cutaneous T‐cell lymphoma had this phenotype. Phenotypic analysis using FCM was thus found to be useful for differential diagnosis of T‐cell and NK‐cell lymphomas.

Adult T-cell leukemia/lymphoma is an aggressive malignant disease associated with regulatory T cells as discussed in some recent reports. We analyzed the expression of FOXP3, a key molecule of regulatory T cells, in adult T-cell leukemia/lymphoma and its association with clinicopathological features. Of 169 adult T-cell leukemia/lymphoma cases examined, 60 (36%) showed FOXP3 expression in lymphoma cells. Morphologically, 22 cases were classified as anaplastic large cell variant and 147 as pleomorphic cell variant. Only 1 (5%) of the anaplastic large cell variant cases and 59/147 (40%) of the pleomorphic cell variant cases expressed FOXP3. Epstein–Barr virus-infected cells were significantly more frequently found in FOXP3(+) cases (23/60; 38%) than in FOXP3(−) cases (12/109; 11%) ( P <0.0001). Cytogenetic analysis showed that FOXP3(+) cases had simpler chromosomal abnormalities than FOXP3(−) cases. Clinically, FOXP3(+) and FOXP3(−) cases did not differ significantly in age distribution, clinical stage, lactate dehydrogenase and calcium in serum and overall survival. However, 8 of 34 FOXP3(+) cases suffered a severe infectious state, an indication of immunosuppression, while only 2 of 62 FOXP3(−) cases did so ( P <0.005). FOXP3 expression in adult T-cell leukemia/lymphoma thus reflects morphological features and is clinically and pathologically associated with an immunosuppressive state.

症例は73歳，男性，糖尿病で治療中。2006年12月8日に転倒して左脛骨・腓骨遠位端骨折を受傷，12月14日にプレートによる骨接合術が行なわれた。12月23日より熱発，術創部からの排膿を認めプレートを抜去，創外固定とした。開放創のまま創処置を行なったがMRSA感染で難治のため2007年1月26日よりマゴットセラピーを週2回，合計6回行ない，引き続き陰圧閉鎖療法を行なった。一方でピン刺入部感染を生じたため創外固定器も除去してシーネ固定とし，3月20日に踵部から足背にかけて切開・排膿を行なった。4月6日よりこの部に対しても計6回のマゴットセラピーと陰圧閉鎖療法を行なった。マゴットの生存環境を確保するため外固定が不十分となり変形治癒となったが，患肢の切断を回避できた。本法は糖尿病性壊疽などの難治性潰瘍の治療法として注目されており，保険適応になれば日本国内でも普及していくものと考えられる。

The World Health Organization classification was used to conduct an analysis of geographic, age, sex, and lesion primarily biopsied/resected distribution of 2260 lymphoid neoplasms diagnosed during 2001-2006 throughout Japan. B-cell neoplasms accounted for 65% of all lymphoid neoplasms, T/natural killer (T/NK)-cell neoplasms for 25% and Hodgkin lymphoma for 7%. The most common type was diffuse large B-cell lymphoma (DLBCL, 33%), followed by follicular lymphoma (18%), and adult T-cell leukemia/lymphoma (ATLL, 10%). The high rate of 18% for follicular lymphoma was similar to that in Western countries (11-33%). T/NK-cell neoplasms accounted for a higher percentage of lymphoid neoplasms in Kyushu (30%) and Okinawa (38%) compared with other areas of Japan (18-20%). Among T/NK-cell neoplasms, ATLL was the most common type in Okinawa (54%) and Kyushu (59%). Extranodal NK/T cell lymphoma was the second most common type of T/NK-cell neoplasms in Okinawa (15%). This epidemiological study shows that the distribution patterns of malignant lymphoma differ especially in Kyushu and Okinawa, the endemic area of human T-cell leukemia/lymphoma virus type 1.

Although approximately 10–20% cases of follicular lymphoma lack BCL2 gene rearrangement, there are few reports having described the alternative genetic aberrations and their association about clinicopathological features. In this study, analysis by Fluorescence in situ hybridization of BCL6 gene aberrations in 100 follicular lymphoma cases without IGH/BCL2 rearrangement resulted in the identification of four subgroups. Group I: BCL6 gene rearrangement (n=41); Group II: BCL6 gene amplification/3q27 gain (n=30); Group III: the absence of both (n=23); and Group IV: the presence of both (n=6). Group II showed higher grade morphology (Grade 3a/b: 93%), higher bcl2 and MUM1 expression (73 and 57%, respectively), and more frequent combination with BCL2 gene amplification/18q21 gain (90%) than the other groups. BCL6 gene aberration, especially amplification/3q27 gain, indicates the presence of certain morphological and phenotypical findings in follicular lymphoma cases without IGH/BCL2 rearrangement.

The aim of the present study was to estimate the relationship between apoptosis and cell proliferation in histiocytic necrotizing lymphadenitis (HNL). Fifteen patients with HNL were retrospectively analyzed. The patients were divided into three groups according to the proportion of the necrotic area as follows: necrosis (+), necrotic area <25%; necrosis (++), necrotic area 25–50%; and necrosis (+++), necrotic area >50%. Immunohistochemical double staining was performed for CD3 plus caspase‐3 and for Ki‐67 plus caspase‐3 and positive cells were counted in two areas: one without and one with obvious apoptotic features. Most caspase‐3‐positive cells were also stained for CD3 (area exhibiting obvious apoptotic features: average, 92.3%). Furthermore, various proportions of both Ki‐67‐ and caspase‐3‐positive cells were detected in all the groups (range, 5–70%). In the area with obvious apoptotic changes, the average percentage of both Ki‐67‐ and caspase‐3‐positive cells (38.6%) was higher than that in the area without obvious apoptotic features (16.3%). A proportion of cells in HNL undergo proliferation and apoptosis simultaneously, such as neoplastic cells, thereby exhibiting rapid cell cycles.

OBJECTIVE:The main histological change in rheumatoid arthritis (RA) is the villous proliferation of synovial lining cells. This seems to be the result of the proliferation and apoptosis induced by immune balance. We studied the involvement of RCAS1 and the infiltration of cytotoxic T lymphocytes (CTL), and examined the synovium immunohistochemically to determine the involvement of proliferation and apoptosis in synovial lining cells, and their relationship with the activity of RATreg cells in the germinal center.METHODS:We used double-immunological staining of Ki-67 and caspase-3 to investigate proliferation and apoptosis. We analyzed CTL, regulatory T cells (Treg), and receptor-binding cancer antigen expressed on SiSo cells (RCAS1), recently recognized to play a role in immune evasion. Proliferation and apoptosis were more frequently encountered in synovial lining cells in RA than in those in osteoarthritis (OA) that were used as a control.RESULTS:High expression of RCAS1 was detected more frequently in the synovial lining cells of OA, but CTL infiltration into the synovium was rarely found. In RA, on the other hand, CTL were observed, while RCAS1 expression was lacking. We compared the presence of Foxp3-positive cells with the level of C-reactive protein (CRP) that served as an active inflammatory marker. Foxp3-positive cells in the germinal center and in CRP showed possible correlation in terms of the range of inflammatory states.CONCLUSION:In RA, the lack of RCAS1 is thought to induce CTL infiltration through loss of the ability to evade immune attack, thus leading to apoptosis of the synovial lining cells. In addition, Treg cells may play a role in the downregulation of activated T cells.

Adult T‐cell leukemia/lymphoma (ATLL) is a human malignancy associated with human T‐cell leukemia virus type 1 (HTLV‐1). The pathological features of the lymph nodes of ATLL change from those of lymphadenitis to Hodgkin's‐like features and those of lymphoma. Chemokines and their receptors are closely associated with T‐cell subgroups and immune responses. To clarify the relationship between chemokines and their receptor expression, as well as the development of ATLL, 17 cases with ATLL were analyzed using DNA chips of chemokines and their receptors. All cases showed a varied and mixed pattern of upregulated and downregulated gene expression of Th1, Th2, naïve, and cytotoxic cell‐associated chemokine genes. As CC chemokine ligand 18 (CCL18) accounted for the most upregulated gene and CX3C chemokine receptor 1 (CX3CR1) for the most downregulated gene, they were selected for immunohistochemical analysis. Immunohistochemical staining showed expression of the two genes in immunological cells, with a positive expression for reticulum cells, but not for ATLL cells. HTLV‐1‐associated lymphadenitis type (n = 13) and Hodgkin's‐like type (n = 12) cases showed significantly higher CCL18 expression than the non‐specific lymphadenitis cases (n = 10) (P < 0.05). However, all HTLV‐1‐associated cases showed significantly lower CX3CR1 expression than the non‐specific lymphadenitis cases (P < 0.05). These results suggest that upregulation of CCL18 expression and downregulation of CX3CR1 expression play a role in immune responses against the ATLL cells. (Cancer Sci 2007; 98: 1875–1880)

Background, Aim and Scope. The Home Appliance Recycling Law (hereunder referred to as the Law) for used cathode ray tube (CRT) TVs, air conditioners, refrigerators and washing machines was enacted in April 2001 in Japan. The Law requires that retailers reclaim, and manufacturers and importers recycle such home appliances. Consumers are required to pay collection and recycling fees incurred in disposing of any of the four home appliances. Home appliances must, as a general rule, be managed in accordance with the Law. In reality, other routes exist, such as via local authorities, scrap processors, illegal dumping and exporting. At about the time the Law was enacted, the refrigerant used for air conditioners and refrigerators was replaced by more environmentally friendly substances such as isobutene. Local authorities had the responsibility of disposing of the appliances of households before the enactment of the Law. It was general practice for local authorities to dispose of home appliances in landfills after breaking them up and recovering valuable resources such as iron, copper and aluminum. Although they made efforts to recover refrigerant fluorocarbons, there were not required to do so.Materials and Methods. This study analyzed the material flow resulting from the Law and other processing flows to quantify the global warming effect caused by home appliance recycling using the life cycle assessment (LCA) method. To evaluate the Law and to develop policy planning, the challenges of future efforts will be considered using time series data. For these reasons, we have assessed the Project Scenario, which corresponded to the present reality; the Baseline Scenario, which assumed that measures such as the Law were not implemented after 2000, and the Ideal Scenario, where all used products were recycled as prescribed by the Law. The environmental impacts for each scenario were estimated using value, which was obtained from multiplying the amount of reproduction and waste treatment by each inventory data.Results. It is estimated that emission reductions of 4.7E+4 t CO(2)e, subtracted the Project Scenario from the Baseline Scenario, were reduced for TVs in 2001 through recycling. The impact from recycling glass from cathode ray tube (CRT) televisions is significant. An improvement of 2.3E+4 t CO(2)e could be anticipated by upgrading to the Ideal Scenario in 2001.It was estimated that there was a reduction of 9.2E+5 t CO(2)e in 2001 for air conditioners. Although the effect of the recovery for refrigerants contributed greatly, some fluorocarbons that are still discharged have had a considerable impact on greenhouse gas emissions. Hypothetically, a reduction of 3.2E+6 t CO(2)e could be anticipated with the Ideal Scenario in 2001.A reduction of 2.6E+6 t CO(2)e was achieved for refrigerators in 2001. Although a further reduction can be anticipated through the Ideal Scenario, there will not be much difference with the Project Scenario by 2010.It was estimated that 3.8E+4 t CO(2)e were reduced for washing machines in 2001. Only a small improvement can be expected through the Ideal Scenario.Discussion. Since many assumptions were used in this study, a sensitivity analysis was carried out in order to grasp their impact. The findings of the sensitivity analysis are that the uncertainties are large, but the number of the greenhouse gas (GHG) reductions is still clear except for the difference between the Project Scenario and the Ideal Scenario for TVs. This analysis gives authenticity to the findings.Conclusions. Establishing a system for liquid crystal display and plasma display panel TVs is desirable because the absolute amount of used LCD/PDP TVs will rapidly increase as the usage of CRT TVs rapidly decreases from 2007.With regard to refrigerant recovery from air conditioners, a significant decrease in GHG emissions has been recorded. There is, however, still ample room for improvement. It will be necessary to switch to refrigerants with low global warming potentials (GWPs) or work more on improving the recovery rate in the future. Alternatives and recovery of fluorocarbons from refrigerators contributed greatly to GHG reductions. The GHG emissions from refrigerator recycling will be minimal whether used refrigerator will be processed legally or not because most used refrigerators will contain natural refrigerants in the near future. The improvement for washing machines was low because it was assumed that their main constituent steel has been previously recycled, and that the plastic recycling rate will not change significantly in the future. An improvement in the recycling technology itself is required. This study was carried out on four home appliance products, and it was found that the Home Appliance Recycling Law has brought significant reductions in GHG emissions. There is also room to make GHG reductions through improving the processing methods further.Recommendations and Perspectives. The impact on GHG emissions by fluorocarbons of air conditioners and refrigerators is the greatest. Adequate measures are particularly required for air conditioners that may continue to discharge GHGs in the future.

End-of-Life Vehicle (ELV) Recycling Law has been ensured since January 2005 and Automobile company and importer have been required to manage fluorocarbons, air-bags and Automobile Shredder Residue (ASR). These companies are changing an ASR treatment method from landfill to incineration with thermal recovery because the law also requires them to increase recycling rate more than 70% of ASR by 2015. This study is to assess these ELV treatment methods to find the effects of the law and important processes to reduce environmental impacts. The assessed ELV treatment methods of this study are a) a shredding and landfill type, b) a shredding and heat recovery type, c) a pressed ELV recycling on electric furnace type and d) pressed ELV recycling on converter type.As a result, fluorocarbons collecting rate and re-use rate of main parts are specified as more important processes for reducing environmental impacts than others. It is found that ELV and ASR transport process are less important. There is no clear difference of environmental impacts among lawful types, though, these types are about 3000 kg-CO2 equiv. less than the traditional type, a) a shredding and landfill type.